Emerging Biological Threats: A Reference Guide

  • 90 1,125 7
  • Like this paper and download? You can publish your own PDF file online for free in a few minutes! Sign Up

Emerging Biological Threats: A Reference Guide


3,737 545 5MB

Pages 342 Page size 336 x 480 pts Year 2009

Report DMCA / Copyright


Recommend Papers

File loading please wait...
Citation preview


This page intentionally left blank




Copyright 2010 by Joan R. Callahan All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, except for the inclusion of brief quotations in a review, without prior permission in writing from the publisher. Library of Congress Cataloging-in-Publication Data Callahan, Joan R. Emerging biological threats : a reference guide / Joan R. Callahan. p. ; cm. Includes bibliographical references and index. ISBN 978-0-313-37209-4 (alk. paper) 1. Emerging infectious diseases. 2. Health risk assessment. 3. Food security. I. Title. [DNLM: 1. Disease Outbreaks—prevention & control. 2. Food Contamination—prevention & control. 3. Hazardous Substances—adverse effects. 4. Public Health—history. WA 105 C156e 2010] RA643.C263 2010 362.196'9—dc22 2009046252 14 13 12 11 10

1 2 3 4 5

This book is also available on the World Wide Web as an eBook. Visit www.abc-clio.com for details. ISBN: 978-0-313-37209-4 EISBN: 978-0-313-37210-0 ABC-CLIO, LLC 130 Cremona Drive, P.O. Box 1911 Santa Barbara, California 93116-1911 This book is printed on acid-free paper Manufactured in the United States of America

Dedicated to my great-grandfather MICHAEL FOLEY (1849–1897) Born during the Irish Famine Died from an experimental tuberculosis treatment

This page intentionally left blank




1. Introduction Public Health: A Short History Koch and His Postulates Hazard, Threat, and Risk Outbreaks, Epidemics, and Pandemics What Is Popular Culture? More Definitions So How Bad Is It?

1 2 2 2 6 6 6 6

2. Five Big Ones HIV Disease and AIDS Malaria Tuberculosis Influenza Hepatitis B and C

9 9 18 25 32 40

3. Five More (and Complications) Measles Dysenteries and Enteric Fevers Dengue and Dengue Hemorrhagic Fever Bad Bugs and Miracle Drugs Emerging Diseases What about Pneumonia? What about Meningitis and Encephalitis? Conclusion

49 49 55 63 69 76 86 92 101

4. Food Insecurity What about Bees?

103 103



Mad Cow Disease Foot-and-Mouth Disease Anthrax Rinderpest Heartwater Classical Swine Fever Blue-Ear Pig Disease Newcastle Disease Avian Influenza Honeybee Colony Collapse Disorder Conclusion

104 109 113 117 120 124 128 132 136 141 146

5. Food Insecurity, Continued Citrus Tristeza Virus Bacterial Wilt Southern Corn Leaf Blight Citrus Canker Late Blight of Potato Soybean Rust Witches’ Broom Disease Phoma Stem Canker Asian Soybean Aphid Locusts Conclusion: One to Grow On

147 147 156 160 163 167 171 174 178 182 186 190

6. Making Things Worse Too Many Babies: Overpopulation Too Much Carbon: Global Climate Change Not Enough Food: Famine, Pestilence, Destruction, and Death Too Much Food: Metabolic Syndrome and Type 2 Diabetes Too Many Sick People: The Healthcare Crisis Too Many Angry People: Bioterrorism Too Many Experts: The Bogus Health Industry Too Many Drugs: Substance Abuse Too Much UV: Stratospheric Ozone Depletion Revisited Too Many Cooks: Environmental Management Issues Conclusion

193 193 199 204 208 212 217 222 227 231 235 241

7. Fighting Back Part 1: Balking the Enemy’s Plans Health Education Better Food A Higher Power Basic Research Water, Toilets, and Garbage Part 2: Preventing the Junction of the Enemy’s Forces Lookouts: Surveillance and Screening Arming the People: Vaccination Holding the Line: Convenient Barriers The Fifth Column: Ringers and Decoys A Clean Camp: Home, School, and Workplace

243 244 244 246 250 252 254 256 257 260 265 268 269


Part 3: Attacking the Enemy’s Army in the Field Killing the Enemy: Snipers and WMDs Disabling the Enemy’s Transportation: Inconvenient Barriers Destroying the Enemy’s Resources: Habitat Modification Enlisting Allies: Biological Controls Bugout: Postexposure Prophylaxis Part 4: Besieging Walled Cities Mopping Up: Disease Eradication and Elimination Occupation: Public Health Enforcement Recruitment: Help Wanted Who’s Going to Pay for This? Tuberculosis: The Million-Year War Postscript: Making Friends Index


272 273 275 278 280 282 284 284 290 292 293 295 297 299

This page intentionally left blank


It is my aspiration that health will finally be seen not as a blessing to be wished for, but as a human right to be fought for. —Attributed to Kofi Annan (1938–)

In the last week of April 2009, the manuscript for this book was nearly finished when reports of the Mexico City swine flu outbreak exploded onto computer and television screens worldwide. Two weeks later, the reported death toll of 150 had declined to 52—not because people came back to life, but because the cause of death was often hard to verify. It was an unusual flu strain that health departments had not seen before, but the news media treated it like the Apocalypse. When revised numbers showed that the new strain was no more deadly than ordinary seasonal flu, the Monday-morning quarterbacking began. Was the public health response appropriate, or was it hype? Was it wrong for the Chinese to quarantine Mexican tourists, or for the Egyptians to slaughter their pigs? But just as public interest showed signs of fizzling, a new headline appeared: “SWINE FLU–HIV COULD DEVASTATE HUMAN RACE.” Worse, the source was not the Weekly World News, but a major wire service1 quoting the head of the World Health Organization. The press release seemed to say that the new H1N1 swine flu strain could combine with the human immunodeficiency virus—the agent of AIDS—to create an airborne threat like nothing the world has ever seen. Many readers took this to mean that the two viruses might physically blend together and give rise to one ugly bug, but as far as we can tell, WHO said nothing of the sort. The original warning posted on the WHO website simply meant that the millions of people living with HIV would be at high risk for complications if they also caught the flu. At the time this book went to press, the H1N1 swine flu outbreak had recently achieved pandemic status. In another year or two, the world will know whether the healthcare system has coped adequately with the result. At present, however, it seems unlikely that this is the longawaited biological Big One. In May 2009, when the media breathlessly reported that N95 face masks were flying off the shelves as a result of high demand for flu protection, the author visited three hardware stores in a medium-sized city near San Diego. The shelves were well stocked with 1. United Press International, 4 May 2009.



N95 particulate respirators as usual, and nobody else seemed interested in them. In theaters and shopping malls and college campuses and buses, no one was wearing a mask. The next day, the top news story was no longer the swine flu, but the fact that a well-known actress had gained weight. These observations corroborated a Gallup poll, which showed that only 8 percent of Americans were worried about the swine flu. The virus was silent, but the people had spoken. And then the people spoke again, in June 2009, this time in the form of a distraught father in upstate New York whose son caught the flu. Blaming the school district for exposing his child to what he perceived as a serious health threat, he stormed the district office and threatened the superintendent with a gun. Fortunately, no one was hurt and the son recovered quickly, but the incident suggested that not everyone was interpreting media reports in the same way. Some people took the exaggerated warnings seriously, while many others ignored the outbreak altogether. Information overload can do that. By late June 2009, an estimated 1 million Americans had contracted the new H1N1 flu strain. Yet only about 3,000 had actually been hospitalized, and 127 had died. A vaccine was in production and would be available by October, but it was unclear how many people would request it, or what direction the pandemic would take. Most biological threats—potentially harmful things of biological origin—are infectious diseases, and influenza is just one of many such diseases that this book discusses in detail. After an introductory chapter that defines some terms and concepts, Chapters 2 and 3 describe ten major human diseases (or disease categories) and related conditions. Each section draws on sources ranging from popular culture and urban legends to the recent biomedical literature. Since biological entities that threaten the food supply are indirect threats to man, Chapters 4 and 5 explore this topic. Chapter 6 examines some human activities that have increased the level of risk associated with certain diseases, and Chapter 7 revisits the war on infectious disease from the perspective of the legendary (perhaps apocryphal) Chinese military strategist Sun Tzu.



All interest in disease and death is only another expression of interest in life. —Thomas Mann, The Magic Mountain

Most people in the Chicago area (and many others worldwide) have heard about the Great Epidemic of 1885, which resulted from a rainstorm that swept raw sewage into Lake Michigan and contaminated the city’s water supply. For decades, historians have reported how an estimated 90,000 people, or one-eighth of the population of Chicago at that time, died of cholera or dysentery in the days that followed. The event has become nearly as famous as the Great Chicago Fire of 1871, and the players are as familiar as Mrs. O’Leary’s cow. The story of the Great Epidemic features a Citizens’ Association that fought for modern sewage treatment; clueless politicians who failed to heed warnings; comic relief in the form of waiters who continued serving oysters in a flooded restaurant; and thousands of helpless victims shoveled into mass graves. It almost sounds like the synopsis of a Hollywood movie, except that there are no movies about diarrhea. But the strangest thing about the Great Epidemic of 1885 is that it never happened. That’s right—the story is an urban legend. (The brave historian who finally debunked the Great Epidemic in 2000 reports that she was met with anger and disbelief.) There are many things that everyone seems to know. Did you hear about the tourist in the Middle East who caught syphilis from a spitting camel? Did you know that malaria is more common in Siberia than in the tropics, so it is not a tropical disease, and global warming will not affect its range? Did you know that Einstein predicted that everybody on Earth will die within four years after honeybees become extinct? And how about the woman who opened a mysterious blue envelope and caught the deadly Klingerman virus? Sorry—camels and llamas do not carry syphilis, malaria is far more common in the tropics than in Siberia, Einstein made no such prediction about bees, and the Klingerman virus doesn’t exist. But the true stories are even better.



PUBLIC HEALTH: A SHORT HISTORY For thousands of years, civil and religious leaders have formulated rules to help people avoid diseases associated with foods, bodily secretions, lifestyle choices, or resource mismanagement. Some of the oldest rules were evidence-based in the modern sense, whereas others were seemingly invented out of thin air. For example, the Bible tells us how Moses stopped an epidemic by ordering the deaths of all foreign women who had “known man by lying with him”—from which one can infer the nature of the disease. The measure was effective, if harsh by modern standards. Moses also enforced a quarantine and ordered the sterilization of clothing and equipment.1 But sometimes public health takes a giant step backwards. Doctors in ancient India treated cholera with good results, by simply rehydrating the patient with herbal potions.2 Later, English colonial doctors brought a belief system that favored more dramatic intervention, such as bloodletting, and the cholera death rate soared. (The English eventually rediscovered the earlier method.) Today, government health agencies have largely assumed the role of high priest in such matters. Public health policies are generally based on scientific evidence rather than divine revelation, but scientists can make mistakes, and individuals have rights too. As a result, governments have limited authority to prosecute those who pose a risk to public health—such as tuberculosis patients who cough in crowded airplanes, parents who refuse to vaccinate their children, people who have unprotected sex with multiple partners, or animal lovers who share their garbage-filled homes with hundreds of cats. Mass execution, in particular, is no longer an option. Despite scientific progress, such topics as food safety, water treatment, and the germ theory of disease itself are hotly debated to this day. Faced with information overload and skyrocketing medical costs, people often must figure out how to take care of themselves and their families. Thus, public health has come full circle. KOCH AND HIS POSTULATES Many statements in this book reflect the premise that certain diseases result from the presence of infectious agents (“germs”) in the body. Familiar examples of germs include bacteria, viruses, parasites, and fungi. Such a disease is called an infectious disease, and this cause-and-effect relationship is generally known as the germ theory of disease. Not everyone subscribes to it, even today; but in 1890 the theory got a big boost from a German doctor named Robert Koch (1843–1910), who figured out a way to prove it. The criteria that he defined are known today as Koch’s Postulates: 1. The microorganism must be present in all organisms with a specific disease. 2. The microorganism must be isolated from a diseased organism and grown in pure culture. 3. The cultured microorganism, when introduced into a healthy organism, must cause the same disease seen in the original organism. 4. The microorganism must be reisolated in pure culture from the experimental host and proven identical to the original specific causative agent. HAZARD, THREAT, AND RISK A biological hazard (or biohazard or BH), as defined in this book, is anything of biological origin that can harm human beings (or their goods or environment). Examples include disease1. Numbers 31:17–24. 2. Sushruta Samhita III, verse II.



causing bacteria and viruses, the toxic chemicals that some plants produce, and the venoms that some insects and reptiles inject when they sting or bite. A biological threat (or biothreat or BT) is about the same thing as a biological hazard, but usually worse. By this definition, a nuclear weapon is not a biological hazard or threat. It certainly qualifies as a hazard or threat, but the weapon itself is not of biological origin. Cancer is not considered a biological hazard either, although some forms of cancer result from exposure to biological hazards, such as certain viruses or tobacco smoke. Some other cancers result from exposure to nonbiological hazards, such as asbestos. Risk is a measure of the expected loss resulting from a given hazard, based on how severe the loss might be and how likely it is to occur. A banana peel on the surface of the moon is a biohazard, in the sense that it is biological in origin and someone might slip on it; but this outcome is quite unlikely, so the risk is near zero. As another example, consider the smallpox vaccine, which can kill about one in every million people who are injected with it. Is this an acceptable risk, or not? That depends on the perceived benefits of protection from a disease that no longer exists. There is a remarkable disconnect between what people are afraid of and what is really dangerous. Surveys have shown, for example, that the ten most feared diseases in the United States include five infectious diseases or categories: “foreign” diseases as a group, “deadly” diseases released by bioterrorists, AIDS, influenza, and Lyme disease (Table 1.1). The first two choices imply that people would prefer to die at the hand of a friend rather than a stranger, which makes sense, sort of. The last two are even less likely causes of death, considering that the mortality rate for influenza is usually less than 0.01 percent and that for Lyme is near zero. What these four diseases have in common is that all have received extensive media publicity. Only one of the diseases in Table 1.1, AIDS, is actually one of the world’s most deadly infectious diseases (Table 1.2). Among the leading causes of death in the United States and other high-income nations (Table 1.3), only one infectious disease, lower respiratory infection—essentially the same thing as pneumonia—even makes the cut. Pneumonia can result from various bacterial or

Table 1.1 Most Feared Diseases, United States, 2003 Disease or Condition Cancer (all forms) Foreign disease such as SARS Deadly disease released by terrorists Heart disease Diabetes Arthritis Stroke High blood pressure AIDS Vision loss Alzheimer’s Hearing loss Emphysema Influenza Parkinson’s Lyme disease Sources: Gallup Organization (survey GO 138154).

Percent “Very Worried” 16 15 15 13 11 11 9 9 7 7 6 5 5 4 3 3



Table 1.2 Top Ten Infectious Diseases, 2002 Disease

Estimated Deaths (Worldwide)

Respiratory infections HIV/AIDS Diarrheal diseases Tuberculosis Malaria Measles Pertussis Tetanus Meningitis Syphilis

3,871,000 2,866,000 2,001,000 1,644,000 1,224,000 645,000 285,000 282,000 173,000 167,000

Source: World Health Organization (WHO), World Health Report 2004.

viral infections, or it can occur as a complication of influenza or other diseases. The other causes of death on this list are noninfectious conditions such as heart disease and cancer. In low-income countries, the annual mortality picture (Table 1.4) is quite different, with five infectious diseases or disease categories ranking among the top ten killers: pneumonia, AIDS, diarrhea, malaria, and tuberculosis. In middle-income countries, two infectious diseases make the list (Table 1.5). In terms of total healthcare costs (Table 1.6), the top ten medical conditions in the United States as of 2008 are heart disease, trauma, cancer, mental disorders, asthma and chronic obstructive pulmonary disease (COPD), high blood pressure, type 2 diabetes, osteoarthritis and other joint diseases, back problems, and normal childbirth. Many of these conditions are related to obesity, lifestyle choices, and the wear and tear of daily living. But notice that there are no infectious diseases on the list—unless, of course, most forms of heart disease and cancer turn out to be infectious after all.

Table 1.3 Top Ten Causes of Death, High-Income Countries, 2002 Disease or Condition Coronary heart disease Stroke and other cerebrovascular diseases Cancers of the trachea, bronchus, or lung Lower respiratory infections Chronic obstructive pulmonary disease (COPD) Cancers of the colon or rectum Alzheimer’s disease and other dementias Diabetes mellitus Cancer of the breast Cancer of the stomach Source: World Health Organization (WHO).

Annual Deaths 1,340,000 770,000 460,000 340,000 300,000 260,000 220,000 220,000 150,000 140,000


Table 1.4 Top Ten Causes of Death, Low-Income Countries, 2002 Disease or Condition

Annual Deaths

Coronary heart disease Lower respiratory infections HIV/AIDS Perinatal conditions Stroke and other cerebrovascular diseases Diarrheal diseases Malaria Tuberculosis Chronic obstructive pulmonary disease Road traffic accidents

3,100,000 2,860,000 2,140,000 1,830,000 1,720,000 1,540,000 1,240,000 1,100,000 880,000 530,000

Source: World Health Organization (WHO).

Table 1.5 Top Ten Causes of Death, Middle-Income Countries, 2002 Disease or Condition

Annual Deaths

Stroke and other cerebrovascular diseases Coronary heart disease Chronic obstructive pulmonary disease Lower respiratory infection HIV/AIDS Perinatal conditions Cancer of the stomach Cancer of the trachea, bronchus, or lung Road traffic accidents Hypertensive heart disease

3,020,000 2,770,000 1,570,000 690,000 620,000 600,000 580,000 570,000 550,000 540,000

Source: World Health Organization (WHO).

Table 1.6 Medical Conditions Ranked by Cost, United States, 2002 Disease or Condition

Annual Cost, in Billions of U.S. Dollars

Heart disease Trauma Cancer Mental disorders Asthma and COPD High blood pressure Type 2 diabetes Osteoarthritis and other joint diseases Back problems Normal childbirth Source: U.S. Agency for Healthcare Research and Quality.

76 72 70 56 54 42 34 34 32 32




OUTBREAKS, EPIDEMICS, AND PANDEMICS About 400 million people in Third World nations contract malaria every year, and about 1 million of those people die of malaria every year. That is a mind-boggling tragedy, but not an epidemic. An epidemic is a sudden increase in the number of cases over the expected number; and the expected number is usually the average number recorded in recent years. An outbreak is similar to an epidemic, except that the affected population is usually smaller and more localized. A pandemic is essentially a worldwide epidemic, but there are other criteria, such as the number of regions affected and the extent to which the disease spreads within each region. (A pandemic is not necessarily dangerous; it depends on what the disease is.)

WHAT IS POPULAR CULTURE? Every major biological threat described in this book has played a role in popular culture, and every section includes examples to illustrate this point. But what is popular culture? There are so many competing definitions that the term itself must have arisen as a product of popular culture. As used here, “popular culture” encompasses not only the arts and entertainment media, but also widely publicized events or beliefs, such as urban legends, Internet myths, hoaxes, rumors, and folk traditions, whether ultimately validated or not.

MORE DEFINITIONS Prions, the smallest known infectious agents, are not alive; they are proteins that seem to cause disease by inducing other proteins to change shape. Viruses are extremely small, probably nonliving entities that can reproduce only inside living cells. A bacterium (plural bacteria) is a small, one-celled organism that has no nucleus and differs in other ways from the cells of animals and plants. Rickettsiae, spirochetes, and chlamydiae are specific types (or relatives) of bacteria. Protozoa are not exactly single-celled animals, as their name might suggest, but close to it. A prion, virus, or bacterium that causes disease is called a pathogen. Protozoa or larger creatures (such as worms) that cause disease are usually called parasites. Infectious diseases are diseases that result from the presence of a pathogen or parasite in the body. A communicable disease is a disease that one host can transmit to another. A host is a human or other organism that a pathogen or parasite uses as a source of food or shelter. If the host acts as a source of infection for other species, it is called a reservoir host. Vectors are insects or other organisms that transmit pathogens between hosts. A zoonosis (plural, zoonoses) is a disease that infects both humans and other vertebrate species.

SO HOW BAD IS IT? The Four Horsemen of the Apocalypse and other images in the Book of Revelation have become powerful nonsectarian symbols for many people. Even the swine flu pandemic of 2009 prompted some millennial thinking, with at least one TV celebrity advising viewers to isolate themselves and to stock up on canned food and bottled water. Is Pestilence (epidemic disease) really the one on the white horse? And if so, can diseases or other biological threats really bring about the end of the world? We can’t comment on the first issue, and as for the second, it all depends on what you mean by “end” and “world.”



If the question is whether any real or imagined biothreat could shatter the Earth’s core, annihilate all living things, and hurl frozen bits of primordial soup screaming into outer space, to begin the long interstellar journey to seed some distant world with the victor’s DNA—no, we don’t see that happening in the near future. Nor do most scientists consider it likely that any single pathogen could destroy all life on Earth, or even drive the human species to extinction. But some diseases and contributing factors do have the potential to end hundreds of millions of individual lives, to transform human societies and economies, and to cause unimaginable hardship to our children and grandchildren. A biothreat, then, is what Lewis Carroll called a portmanteau word—two words packed into one, like a portmanteau suitcase with two compartments. But what is inside? Whatever you take with you. Reading about biothreats really means confronting your worst nightmare, and every reader has a different one. Whether you fear paralysis, asphyxiation, pain, bleeding, disfigurement, infertility, starvation, or just plain death, rest assured that it’s somewhere in this book.

References and Recommended Reading Ackerman, G. A., and J. Giroux. “A History of Biological Disasters of Animal Origin in North America.” Revue Scientifique et Technique, Vol. 25, 2006, pp. 83–92. Ackerman, G. A. “It Is Hard to Predict the Future: The Evolving Nature of Threats and Vulnerabilities.” Revue Scientifique et Technique, Vol. 25, 2006, pp. 353–360. Beran, G. W. (Ed.) 1994. Handbook of Zoonoses. Boca Raton, FL: CRC Press. Booker, C., and R. North. 2008. Scared to Death: From BSE to Global Warming—How Scares Are Costing Us the Earth. London: Continuum. Brown, L. R., and B. Halwell. “Breaking Out or Breaking Down.” World Watch, Vol. 12, 1999, pp. 20–29. Callahan, J. R. 2002. Biological Hazards: An Oryx Sourcebook. Westport, CT: Oryx Press (imprint of Greenwood Publishing Group). Delamothe, T. “Several Horsemen of the Apocalypse.” British Medical Journal, Vol. 337, 2008, p. a1365. Fielding, J. E. “Public Health in the Twentieth Century: Advances and Challenges.” Annual Review of Public Health, Vol. 20, 1999, pp. xiii–xxx. Gillett, J. D. “The Behaviour of Homo sapiens, the Forgotten Factor in the Transmission of Tropical Disease.” Transactions of the Royal Society of Tropical Medicine and Hygiene, Vol. 79, 1985, pp. 12–20. Goleman, D. “Hidden Rules Often Distort Ideas of Risk.” New York Times, 1 February 1994. Guadalupe, P., and L. Saad. “Public Perceptions of Worldwide Malaria and TB Risks Haven’t Risen.” Gallup News Service, 26 June 2007. Hiiemäe, R. “Handling Collective Fear in Folklore.” Folklore, Vol. 26, 2004, pp. 65–80. Hill, L. 2000. The Chicago River: A Natural and Unnatural History. Chicago: Lake Claremont Press. Hill, L. “The Chicago Epidemic of 1885: An Urban Legend?” Journal of Illinois History, Vol. 9, 2006, pp. 154–174. Jackson, J. W. “Bioterrorist Attacks on Food Would Cause More Panic than Actual Damage.” Knight Ridder/ Tribune Business News, 6 March 2003. Jones, K. E., et al. “Global Trends in Emerging Infectious Diseases.” Nature, Vol. 451, 2008, pp. 990–993. Kumate, J. “Infectious Diseases in the 21st Century.” Archives of Medical Research, Vol. 28, 1997, pp. 55–61. Lane, J. M., et al. “Deaths Attributable to Smallpox Vaccination, 1959 to 1966, and 1968.” Journal of the American Medical Association, Vol. 212, 1970, pp. 441–444. Lopez, A. D., et al. “Global and Regional Burden of Disease and Risk Factors, 2001: Systematic Analysis of Population Health Data.” Lancet, Vol. 367, 2006, pp. 1747–1757. Lorber, B. “Are All Diseases Infectious?” Annals of Internal Medicine, Vol. 125, 1996, pp. 844–851. Maugh, T. H. “Worldwide Study Finds Big Shift in Causes of Death.” Los Angeles Times, 16 September 1996. McMichael, A. J. “Environmental and Social Influences on Emerging Infectious Diseases: Past, Present and Future.” Philosophical Transactions of the Royal Society of London B, Vol. 359, 2004, pp. 1049–1058.



Moeller, S. D. 1999. Compassion Fatigue: How the Media Sell Disease, Famine, War, and Death. New York: Routledge. Ong, A. K., and D. L. Heymann. “Microbes and Humans: The Long Dance.” Bulletin of the World Health Organization, Vol. 85, 2007, pp. 422–423. Patz, J. A., et al. “Unhealthy Landscapes: Policy Recommendations on Land Use Change and Infectious Disease Emergence.” Environmental Health Perspectives, Vol. 112, 2004, pp. 1092–1098. Sanders, J. W., et al. “The Epidemiological Transition: The Current Status of Infectious Diseases in the Developed World versus the Developing World.” Science Progress, Vol. 91, 2008, pp. 1–37. Slingenbergh, J., et al. “Ecological Sources of Zoonotic Diseases.” Revue Scientifique et Technique, Vol. 23, 2004, pp. 467–484. Smith, D. F. “Food Panics in History: Corned Beef, Typhoid, and ‘Risk Society.’” Journal of Epidemiology and Community Health, Vol. 61, 2007, pp. 566–570. Snowden, F. M. “Emerging and Reemerging Diseases: A Historical Perspective.” Immunological Reviews, Vol. 225, 2008, pp. 9–26. Strange, R. N., and P. R. Scott. “Plant Disease: A Threat to Global Food Security.” Annual Review of Phytopathology, Vol. 43, 2005, pp. 83–116. Trust for America’s Health. “New Report Finds Rising Risk of Infectious Diseases in America.” Press release, 29 October 2008. “UPI Poll: Bioterrorism Seen as Top Threat.” United Press International, 23 February 2007. Weiss, R. A. “The Leeuwenhoek Lecture 2001: Animal Origins of Human Infectious Disease.” Philosophical Transactions of the Royal Society of London B, Vol. 356, 2001, pp. 957–977. Weiss, R. A., and A. J. McMichael. “Social and Environmental Risk Factors in the Emergence of Infectious Diseases.” Nature Medicine, Vol. 10, 2004, pp. S70–S76. Whipple, D. “Microbes Replace Wolves in Culling Herds.” UPI Science News, 1 September 2003.


Five Big Ones

We could easily be made to believe that nothing has happened, and yet we have changed, as a house changes into which a guest has entered. —R. M. Rilke, Letters to a Young Poet (1904)

This chapter discusses the five infectious diseases that (arguably) pose the greatest threat to humans at present. The first three are the ones that top almost everyone’s list: HIV/AIDS, malaria, and tuberculosis. Goal 6 of the United Nations Millennium Project (Table 2.1) is to combat these three diseases. Targeted milestones include halting their spread, and perhaps reducing the numbers of new cases, by 2015. Each of these diseases kills over 1 million people every year worldwide. As of 2009, there is no effective vaccine for HIV/AIDS. There are experimental vaccines for malaria, and an unsatisfactory 90-year-old vaccine for tuberculosis. But HIV is now manageable as a chronic condition, and most cases of TB and malaria are potentially curable—in those patients who have access to expensive and prolonged treatment. As a result, the worst diseases in the world are no longer the ones that the public fears the most. In a 2007 Gallup survey, only 24 percent of U.S. respondents felt that either tuberculosis or malaria was a very serious global health problem (Table 2.2), despite the high death tolls of these diseases. In addition to the “Big Three,” this chapter covers two other diseases that claim between 500,000 and 1 million human lives in a typical year: influenza (all types and subtypes) and hepatitis (types B and C).

HIV DISEASE AND AIDS Summary of Threat The human immunodeficiency virus (HIV) attacks the immune system and makes the body unable to fight infection. Transmission is by fluid exchange. Without treatment, most (not all) people develop full-blown acquired immunodeficiency syndrome (AIDS) and die from opportunistic



infections or cancer within a few years. As of 2009, no effective vaccine or cure is available, but antiretroviral drugs can prolong life and help prevent transmission.

Other Names In the early 1980s, HIV was known as human T-cell lymphotropic virus type 3 (HTLV-III or HTLV-3) or lymphadenopathy-associated virus (LAV). The name HTLV-3 reflected an early hypothesis that the virus was related to the HTLV-1 and HTLV-2 viruses, which cause certain forms of human leukemia. Two labs identified the new virus in 1983 and named it human immunodeficiency virus (HIV). The U.S. Centers for Disease Control and Prevention (CDC) first referred to the disease as acquired immunodeficiency syndrome (AIDS) in 1982. Other names in that era included chronic symptomatic HIV infection, Kaposi’s sarcoma and opportunistic infections (KSOI), and community-acquired immune dysfunction. The term AIDS-related complex Table 2.1 United Nations Millennium Project, Goal 6 Goal 6: Combat HIV/AIDS, Malaria, and Other Diseases Target 7. Have halted by 2015, and begun to reverse, the spread of HIV/AIDS Indicators 18. HIV prevalence among pregnant women aged 15–24 years (UNAIDS-WHO-UNICEF) 19. Condom use rate of the contraceptive prevalence rate (UN Population Division) 19a. Condom use at last high-risk sex (UNICEF-WHO) 19b. Percentage of population aged 15–24 years with comprehensive correct knowledge of HIV/AIDS (UNICEF-WHO) 19c. Contraceptive prevalence rate (UN Population Division) 20. Ratio of school attendance of orphans to school attendance of non-orphans aged 10–14 years (UNICEF-UNAIDS-WHO) Target 8. Have halted by 2015, and begun to reverse, the incidence of malaria and other major diseases Indicators 21. Prevalence and death rates associated with malaria (WHO) 22. Proportion of population in malaria-risk areas using effective malaria prevention and treatment measures (UNICEF-WHO) 23. Prevalence and death rates associated with tuberculosis (WHO) 24. Proportion of tuberculosis cases detected and cured under DOTS (internationally recommended TB control strategy) (WHO) Source: United Nations.

Table 2.2 Perceptions of Global Health Issues, United States, 2007 Very Serious %

Somewhat Serious %

Not Serious %

82 79 75 24 24

16 20 22 51 50

2 1 3 23 22

HIV/AIDS Cancer Poor nutrition Tuberculosis Malaria Source: Gallup News Service.



(ARC) refers to milder symptoms of HIV infection, such as weight loss and enlarged lymph nodes. In French- and Spanish-speaking countries and communities, the translation of AIDS is abbreviated SIDA. In the early 1980s, the media coined several pejorative or inaccurate names, such as gayrelated immunodeficiency disease (GRID), gay cancer, gay compromise syndrome, gay plague, and—most offensive of all—the so-called 4-H Club (Haitians, hemophiliacs, heroin users, and homosexuals). Other slang terms for AIDS that appear to assign blame include “women’s disease” and “men’s disease,” both used in Tanzania. But Africans also call HIV/AIDS by names that are highly descriptive in translation, such as “slim disease” (Kenya), “that which came” (Zimbabwe), “lack of guard in the body” (Tanzania), “a thing that sucks life out” (Uganda), “God is tracking you” (South Africa), “those that suffer from the germ” (Zambia), “stepped on a landmine” (Angola), or simply “death” (Nigeria).

Description HIV (Figure 2.1) is one of the retroviruses—a group of RNA viruses that can copy their genetic material into DNA, which then becomes part of a host cell chromosome. HIV exists in

Figure 2.1 Scanning electron micrograph showing human immunodeficiency virus (HIV-1, small spherical objects) and human lymphocytes. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



at least two forms, known as HIV-1 and HIV-2. The predominant form in most of the world is HIV-1, which includes three groups designated as M, N, and O. In 2009, French researchers identified a fourth group (tentatively designated as HIV-1 group P) that is closely related to a virus found in gorillas. Group M, the cause of most HIV-1 infections, comprises several genetic subtypes known as clades. Thanks to its devastating effects and extensive media coverage, HIV/AIDS is perhaps better known to the American public than any other infectious disease. Yet the chief modes of HIV transmission are worth repeating: sexual contact (either homosexual or heterosexual) with exchange of body fluids; needle sharing by intravenous drug users; blood transfusions, organ transplants, or other medical procedures; laboratory transfer, such as needlestick injuries or splashing of contaminated body fluids on a skin lesion; or transfer during pregnancy or birth. The virus cannot replicate itself in mosquitoes, bedbugs, or ticks, so it is highly unlikely that these insects can serve as vectors. The virus can, however, survive for at least eight days in a bedbug or ten days in a tick. Within the first few months after infection with HIV, many people develop a mild illness that lasts for a week or two, with symptoms such as fever, fatigue, and swollen lymph nodes. Otherwise, the person may be free of symptoms for several years while the virus silently destroys his or her immune system. Diagnosis requires blood testing for HIV antibodies (which are undetectable for at least a month after infection) or circulating HIV antigen. By the time HIV-related cancers or opportunistic infections (Figure 2.2) appear, it may be too late for antiretroviral drugs to be fully effective, and partners or other contacts may have contracted the disease. The actual cause of AIDS-related death is often an infection such as tuberculosis or Pneumocystis pneumonia.

Figure 2.2 Oral Kaposi’s sarcoma lesion and candidiasis (thrush) in HIV-positive patient. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



Who Is at Risk? Unprotected sex (without a condom) and contaminated needles account for most cases. Risk factors include coinfection with syphilis or other diseases that cause open sores through which the virus can enter. Circumcision may reduce HIV risk, at least in heterosexual men. Herpesvirus6, which causes a childhood disease called roseola, appears to speed up the progress of HIV. Persons of European descent with a gene called Delta32 are resistant to HIV. Another gene, called DARC (Duffy antigen receptor for chemokines), common among West Africans, increases the risk of HIV while conferring some protection against malaria. About two-thirds of all HIV cases, and three-quarters of all AIDS-related deaths, are in sub-Saharan Africa. Infection with HIV also increases the risk of contracting other infectious diseases, such as tuberculosis, visceral leishmaniasis, malaria, and many opportunistic infections that do not normally occur in healthy persons, including certain forms of pneumonia.

The Numbers As of 2008, men who have sex with men (MSM) account for about 44 percent of AIDS cases in the United States, 65 percent in Canada, and 64 percent in Australia. These numbers do not imply that homosexuals are at disproportionate risk, but only that the first infected persons in North America and Australia were homosexual, and they transmitted the disease primarily to other homosexuals. In Africa, AIDS occurs mainly in heterosexuals, and about 60 percent of reported cases are in women. Between 1981 and 2008, an estimated 32 million people died of AIDS, including 566,000 in the United States alone. The number of HIV-related deaths peaked in the United States in 1995, while worldwide numbers continued to rise. Recent projections are all over the map, but a 2008 WHO report states that annual HIV/AIDS deaths will peak at 2.4 million in 2012, up from 2.2 million in 2008. By a previous estimate, total deaths would peak at 6.5 million in 2030. These estimates are based on the best available data and assumptions, which change continually. The numbers do not include deaths from “new variant famine,” a term recently applied to hunger that affects African households when one or more family members have AIDS and cannot work. As of 2008, an estimated 33 million people worldwide were HIV-positive, including about 1 million in the United States. About half of all infected U.S. residents were African American, although this group represented only about 12 percent of the total population. By 2008, AIDS had become the leading cause of death among young African American women.

History Researchers believe that retroviruses similar to HIV have existed for millions of years and were present in the earliest primates. HIV-1 probably originated in central Africa in about 1930 and spread to Haiti and the United States during the 1960s. Rumors of a new disease circulated in American prison populations in the 1970s, but the general public did not become aware of the epidemic until 1981, when doctors reported an unusual outbreak of Pneumocystis pneumonia among gay males in California. By then, HIV was established on every continent. The French researchers who identified the virus in 1983, Françoise Barre-Sinoussi and Luc Montagnier, shared the 2008 Nobel Prize in Physiology or Medicine. Since then, research has focused on the development of antiretroviral drugs and vaccines.



The AIDS era has been a time of great discoveries as well as great frustration regarding human rights and priorities. One example will suffice here: In July 2008, President George W. Bush reauthorized the 2003 PEPFAR (President’s Emergency Plan for AIDS Relief) by signing into law the Tom Lantos and Henry J. Hyde United States Global Leadership against HIV/AIDS, Tuberculosis, and Malaria Reauthorization Act of 2008. In theory, this law ends a longstanding ban on HIV-positive travelers entering the United States; however, U.S. immigration law already prohibits foreigners with any communicable disease of public health importance from entering the country. As of 2008, it is not clear how much of a difference the new law will make, except that persons with HIV will no longer be singled out for exclusion. Prevention and Treatment The Bush administration (2001–2009) reportedly spent $6 billion per year to fight AIDS in Africa, but the program focused on antiretroviral drugs rather than prevention. The only known ways to avoid HIV are to avoid sex, needles, contact with injured people, and other potential sources of exposure, or to wear a condom or other protection whenever exposure might occur. Since some belief systems or personal preferences discourage men from using condoms, recent effort has focused on the development of protective barriers for women, such as antiviral gels. As of 2009, these products are still on the drawing board. Female condoms are available, but their high cost and complexity may interfere with acceptance. Improved male condoms would also be beneficial; for example, the spermicide coatings may cause irritation that increases the probability of HIV transmission if the condom breaks. Unfortunately, HIV vaccine trials to date have been unsuccessful or inconclusive. In 2003, a study of several thousand volunteers in North America, Europe, and Thailand concluded that a VaxGen vaccine was ineffective. In 2009, however, shortly before this book went to press, preliminary reports indicated that a VaxGen vaccine used in combination with a second vaccine appeared to reduce new HIV infections by about 30 percent. In 2007, a Merck vaccine failed in a study of 3,000 volunteers in nine countries. Clinical trials of a vaccine called Remune® yielded inconclusive results, and the manufacturer filed bankruptcy in 2008. As of 2009, HIV treatment requires a combination of drugs: reverse transcriptase inhibitors to stop the virus from building new DNA, protease inhibitors to interfere with the action of viral enzymes, and fusion inhibitors to stop HIV from entering the host cell membrane. This treatment (called highly active antiretroviral therapy or HAART) has prolonged and improved many lives, but it often has side effects, such as nausea, vomiting, and diarrhea. Less frequent outcomes include diabetes, liver failure, pancreatitis, and enlargement of the breast or neck. Antiretroviral drugs can also cause immune restoration inflammatory syndrome (IRIS), in which opportunistic infections temporarily return. Some of the same drugs are used for short-term post-exposure prophylaxis (PEP), to treat people who have been exposed to HIV. Unfortunately, drug-resistant HIV strains have already appeared (Chapter 3). There are recent reports of individuals who have apparently been cured of HIV by means of bone marrow transplants. These findings are encouraging, but even if this method works, it would be impractical on a large scale. In the near term, management of this disease will continue to focus on antiretroviral drugs, despite the side effects and the staggering cost of treatment. Popular Culture Any disease as deadly as AIDS becomes a nexus for exaggerated fears and rumors. Many of these misconceptions originated before science established that HIV is not transmitted by casual contact. Under the circumstances, it was reasonable to fear people with an unfamiliar disease that was known to be contagious.


The fear of HIV transmitted by accidental needlestick injury—which really happens on occasion—has given us the urban legend of Needle Boy, who supposedly hides HIV-infected needles in movie theater seats, coin return slots of public phones, and gas pump handles to stick the unwary. Typhoid Mary (Chapter 3) is the prototype for the urban legend of AIDS Mary, who picks up men in bars and infects them with HIV. Ironically, the real Typhoid Mary meant no harm; she simply refused to believe that typhoid is contagious, just as some people nowadays are in denial about HIV. (For examples of HIV denial, see Case Studies 2-1 and 2-2.) In a 2007 Pew opinion survey, a startling 23 percent of Americans agreed with the statement “AIDS might be God’s punishment for immoral sexual behavior.” In 1987, 43 percent of Americans agreed with the same statement. But the wording of the question might be at fault, because almost anything might be true. Some journalists and clergymen have attributed the AIDS epidemic to another authority figure, namely the United States government. One theory holds that doctors administering polio vaccine in Africa accidentally transferred the virus from chimpanzees to humans. Another claims that government agents created HIV as a genocidal weapon against Africans. In a third version, the government used gay American males as guinea pigs for an experimental hepatitis B vaccine that was contaminated with HIV and human herpesvirus-8 (the agent of Kaposi’s sarcoma). These frightening scenarios have not held up to scrutiny, but the rumors continue. Hollywood depictions of AIDS have varied in accuracy and sensitivity. Some critically acclaimed examples are Longtime Companion (1990), Philadelphia (1993), And the Band Played On (1993), and Jeffrey (1995). On a lighter note, the 1987 motion picture Return to Salem’s Lot features a group of vampires who raise cows as a source of blood because of the danger of contracting AIDS or other diseases from human blood. Although the world has been aware of HIV/AIDS for less than 30 years, alleged folk cures already exist, particularly in Africa and Latin America. Perhaps worst of all is the belief that having sex with a virgin will cure AIDS.

Case Study 2-1: HIV and the Down-Low There is no way to address this controversial topic without offending someone, but it’s too important to skip. The “down-low” is a slang term for a phenomenon that has plagued the African American community for decades and has probably caused many unnecessary deaths. The term refers to closeted sexual contact between men who do not regard themselves as homosexual and often do not use protection or seek HIV testing. Because of the difficulty of obtaining accurate data, it is unclear whether such behavior has been a major factor in the spread of HIV. But any source of denial that discourages people from checking their HIV status is one more barrier to defeating the epidemic. Anyone who engages in highrisk behavior must be tested, for the sake of their families and communities.

Case Study 2-2: HIV in Kyrgyzstan Many people apparently still believe that AIDS is 100 percent avoidable by virtuous living, despite evidence to the contrary. In 2008, the news media reported a tragic story that took place in the central Asian republic of Kyrgyzstan. A seven-month-old baby boy developed a high fever, and his mother took him to the local hospital for treatment. At the hospital, the boy contracted HIV from a contaminated intravenous needle, but the hospital did not discover the problem immediately. Meanwhile, the mother took the baby home and continued breastfeeding. Later, both mother and child became ill and tested positive for HIV. It is not clear whether the virus entered through the mammary duct or through a small cut on her breast, but in either case, the mother caught HIV from her baby. Yet the woman's husband allegedly responded by accusing her of adultery, beating her up, and throwing her out of the house along with their son. One such incident would be dreadful enough, but the media reported that at least 72 children and 16 mothers were infected as a result of tainted blood transfusions or reused needles in two Kyrgyz hospitals.




Obviously, this won’t work—it will more likely transmit HIV to the virgin, thus threatening two lives instead of one. This belief is not unique to AIDS; a century ago, European men reportedly sought out virgins to cure syphilis. According to another theory, sex with an animal will cure AIDS or other sexually transmitted diseases, because animals (like virgins) are said to be innocent. Other questionable AIDS cures include bee venom, apple cider vinegar, beet root with garlic, rattlesnake meat, and “AIDS nosode” (plain water mixed with a microscopic quantity of blood drawn from a deceased AIDS patient).

The Future Someday scientists will create an effective HIV vaccine, and the world will rejoice. But will everyone who needs this vaccine choose to accept it? History has taught many people to fear new vaccines. In the 1950s, the first polio vaccines caused polio in hundreds of children, because the attenuated virus was not attenuated enough; and in 1942, some 50,000 U.S. military personnel received a yellow fever vaccine contaminated with hepatitis B. Even the smallpox vaccine that freed the world from that disease did so at the cost of many lives. Also, requesting HIV vaccination or testing might be seen by some as tantamount to an admission of risk. By analogy, an effective vaccine for hepatitis B—a virus with a similar transmission pattern—has been available for nearly 30 years, yet many people have rejected it or have never heard of it. As a result, the hepatitis B epidemic continues (Chapter 3). Until recently, it seemed unlikely that HIV could be eradicated without effective and mandatory vaccination. In 2008, however, WHO researchers published a mathematical simulation that appears to show that HIV transmission could be eliminated in as little as ten years, even without a vaccine. The plan is to test people every year and immediately give them antiretroviral drugs if they test positive. Implementation would pose some major practical problems, but the concept is intriguing (Case Study 7-16, Chapter 7). Because of its effect on the human immune system, HIV poses at least one unique threat that may outlive the virus itself. Before the HIV epidemic, opportunistic infections such as Pneumocystis pneumonia were rare. But now that these pathogens can multiply and undergo mutation in millions of immunosuppressed human hosts, they may evolve into forms that can also infect healthy people. There is no proof that this has happened yet, but it is possible in theory. For that matter, HIV itself could eventually mutate to a form that is transmissible by casual contact, if it continues to circulate unchecked.

References and Recommended Reading “AIDS Rates Among U.S. Blacks Rival Africa.” Science Online, 29 July 2008. Alexaki, A., et al. “Cellular Reservoirs of HIV-1 and Their Role in Viral Persistence.” Current HIV Research, Vol. 6, 2008, pp. 388–400. Altman, L. K. “Rare Cancer Seen in 41 Homosexuals.” New York Times, 3 July 1981. Bartelsman, M., and H. Veeken. “The HIV Pandemic in the Year 2007, an Overview.” Nederlands Tijdschrift voor Geneeskunde, Vol. 151, 2007, pp. 2655–2660. [Dutch] Bhavan, K. P., et al. “The Aging of the HIV Epidemic.” Current HIV/AIDS Reports, Vol. 5, 2008, pp. 150–158. Bockarie, M. J., and R. Paru. “Can Mosquitoes Transmit AIDS?” PNG Medical Journal, Vol. 39, 1996, pp. 205–207. Boykin, K., and E. L. Harris. 2006. Sex, Lies, and Denial in Black America. New York: Carroll and Graf. “California Prisons Giving Inmates Free Condoms.” KNBC.com, 31 July 2008. “CDC: More than 1 Million Have HIV in U.S.” United Press International, 2 October 2008. Cohan, G. R. “Another Bioterrorist.” The Advocate, 4 December 2001.



Cohen, M. S., et al. “The Spread, Treatment, and Prevention of HIV-1: Evolution of a Global Pandemic.” Journal of Clinical Investigation, Vol. 118, 2008, pp. 1244–1254. Cohn, S. K., and L. T. Weaver. “The Black Death and AIDS: CCR5-Delta32 in Genetics and History.” QJM, Vol. 99, 2006, pp. 497–503. Correll, T. C. “‘You Know About Needle Boy, Right?’ Variation in Rumors and Legends about Attacks with HIV-Infected Needles.” Western Folklore, Winter 2008, pp. 59–100. De Waal, A., and Whiteside, A. “New Variant Famine: AIDS and Food Crisis in Southern Africa.” Lancet, Vol. 362, 2003, pp. 1234–1237. Duran, D., et al. “Persons Tested for HIV—United States, 2006. Morbidity and Mortality Weekly Report, Vol. 57, 2008, pp. 845–849. European Centre for Disease Prevention and Control. “HIV Prevention in Europe: Action, Needs and Challenges.” Meeting Report, Stockholm, 2–3 October 2006. Gaym, A. “Microbicides—Emerging Essential Pillars of Comprehensive HIV/AIDS Prevention.” Ethiopian Medical Journal, Vol. 44, 2006, pp. 405–415. Gilbert, M., et al. “The Emergence of HIV/AIDS in the Americas and Beyond.” Proceedings of the National Academy of Sciences, Vol. 104, 2007, pp. 18566–18570. Gottlieb, G. J., et al. “A Preliminary Communication on Extensively Disseminated Kaposi’s Sarcoma in Young Homosexual Men.” American Journal of Dermatopathology, Vol. 3, 1981, pp. 111–114. Hall, H. I., et al. “Estimation of HIV Incidence in the United States.” Journal of the American Medical Association, Vol. 300, 2008, pp. 520–529. Hammer, S. M., et al. “Antiretroviral Treatment of Adult HIV Infections: 2008 Recommendations of the International AIDS Society—USA Panel.” Journal of the American Medical Association, Vol. 300, 2008, pp. 555–570. Humphery-Smith, I., et al. “Evaluation of Mechanical Transmission of HIV by the African Soft Tick, Ornithodoros moubata.” AIDS, Vol. 7, 1993, pp. 341–347. Iqbal, M. M. “Can We Get AIDS from Mosquito Bites?” Journal of the Louisiana State Medical Society, Vol. 151, 1999, pp. 429–433. Jaffe, H. W., et al. “The Reemerging HIV/AIDS Epidemic in Men Who Have Sex with Men.” Journal of the American Medical Association, Vol. 298, 2007, pp. 2412–2414. Lacey, M. “Back from the US and Spreading HIV in Mexico.” International Herald Tribune, 16 July 2007. Laurencin, C. T., et al. “HIV/AIDS and the African-American Community: A State of Emergency.” Journal of the American Medical Association, Vol. 100, 2008, pp. 35–43. Leigh, J. P., et al. “Costs of Needlestick Injuries and Subsequent Hepatitis and HIV Infection.” Current Medical Research and Opinion, Vol. 23, 2007, pp. 2093–2105. Marsden, M. D., and J. A. Zack. “Eradication of HIV: Current Challenges and New Directions.” Journal of Antimicrobial Chemotherapy, 4 November 2008. “Math Model: HIV Can Be Eliminated in a Decade.” Associated Press, 25 November 2008. McGroarty, P. “Doctors Say Marrow Transplant May Have Cured AIDS.” Associated Press, 13 November 2008. Merson, M. H., et al. 2008. “The History and Challenge of HIV Prevention.” Lancet, Vol. 372, 2008, pp. 475-488. “New Hope on AIDS in Africa.” Associated Press, 1 December 2008. Russell, S. “Unsettling Re-emergence of ‘Gay Cancer.’” San Francisco Chronicle, 12 October 2007. “Scientists Lose Hope Over AIDS Vaccine.” Science Online, 24 April 2008. Shafer, R. W., and J. M. Schapiro. “HIV-1 Drug Resistance Mutations: An Updated Framework for the Second Decade of HAART.” AIDS Reviews, Vol. 10, 2008, pp. 67–84. Shin, L. Y., and R. Kaul. “Stay it with Flora: Maintaining Vaginal Health as a Possible Avenue for Prevention of Human Immunodeficiency Virus Acquisition.” Journal of Infectious Diseases, Vol. 197, 2008, pp. 361–368. Singh, M. “No Vaccine Against HIV Yet—Are We Not Perfectly Equipped?” Virology Journal, Vol. 3, 2006, p. 60. “U.N. Agency Lowers AIDS Estimates.” Science Online, 20 November 2007. U.S. Centers for Disease Control and Prevention. 1981. “Kaposi’s Sarcoma and Pneumocystis Pneumonia among Homosexual Men—New York City and California.” Morbidity and Mortality Weekly Report, Vol. 30, 1981, pp. 305–308. Walker, B. D., and D. R. Burton. “Toward an AIDS Vaccine.” Science, Vol. 320, 2008, pp. 760–764.



Weiss, R. A. “The Leeuwenhoek Lecture 2001: Animal Origins of Human Infectious Disease.” Philosophical Transactions of the Royal Society of London B, Vol. 356, 2001, pp. 957–977. Weiss, R. A. “The Discovery of Endogenous Retroviruses.” Retrovirology, 3 October 2006. Willyard, C. “Circumcision Strategy Against HIV Continues to Prove Divisive.” Nature Medicine, Vol. 14, 2008, p. 895. Worobey, M., et al. “Direct Evidence of Extensive Diversity of HIV-1 in Kinshasa by 1960.” Nature, Vol. 455, 2008, pp. 661–664.

MALARIA Summary of Threat Malaria parasites reproduce in the body and invade blood cells, causing severe illness that may recur. As of 2009, there is no commercially available vaccine, and over 1 million people (mostly children in Africa) die from this disease each year. Antimalarial drugs and hospital treatment could save most of them. Since mosquitoes transmit malaria, mosquito control is also essential.

Other Names The parasite Plasmodium falciparum causes the most severe form of malaria, also called falciparum malaria or malignant tertian malaria. Milder forms called benign tertian malaria, quartan malaria, and ovale malaria result from infection with the related species Plasmodium vivax, P. malariae, and P. ovale, respectively. The simian malaria parasite (P. knowlesi) also infects humans in southeast Asia. Mixed infections with more than one parasite species are fairly common. Double tertian malaria or quotidian fever means either infection with two Plasmodium species or two distinct generations of parasites that mature asynchronously, producing daily attacks of fever and chills. Malaria originally meant “bad air” in Italian. In the old days, doctors believed that poisonous vapors rising from swamps caused disease. Malaria was known as swamp fever, marsh fever, marsh miasma, paludism, paludeen fever, paludal fever, Roman fever, Chagres fever, Panama fever, West African fever, malarial fever, jungle fever, congestive fever, remitting fever, biduoterian fever, aestivoautumnal fever, blackwater fever, or ague. “Blackwater” refers to the presence of hemoglobin in the urine, whereas ague is a less specific term for the chills that are often a prominent feature of this disease. Description The infectious agents of malaria are not bacteria or viruses, but single-celled parasites called protozoans. Malaria does not spread directly from one person to another; in most cases, mosquitoes act as vectors. Some cases also result from contaminated needles or blood transfusions. The malaria parasite (Figure 2.3) cannot live independently without a host. It spends part of its life cycle inside a female Anopheles mosquito, where the sexual stages unite, giving rise to cells called sporozoites that migrate to the mosquito’s salivary glands. When the mosquito bites a human to obtain blood, it sprays the bite area with infected saliva. The sporozoites then enter the human bloodstream and find their way to the liver, where they pass through a series of developmental stages and finally reproduce in red blood cells (Figure 2.4). The next time a mosquito bites the infected person, it ingests blood that contains sexual stages of the parasite, and the cycle starts over.

Figure 2.3 Micrograph showing mixed Plasmodium falciparum and P. malariae parasitic infection. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

Figure 2.4 Life cycle of Plasmodium, the parasite that causes malaria. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



Case Study 2-3: A Death in Palm Springs In the spring of 2004, wildlife biologists in California were shocked to learn that malaria had claimed the life of a respected colleague. Although malaria kills many people in Third World nations, death is a rare outcome for malaria patients in American hospitals. The biologist had recently returned to California from a visit to Uganda, where he worked outdoors without using antimalarial drugs. A twoday history of fever and chills brought him to the hospital ER, where he was first diagnosed with Plasmodium malariae (quartan malaria). But after four days of unsuccessful treatment with chloroquine and primaquine, he developed respiratory distress and was transferred to the ICU. A second blood test revealed a mixed infection with P. malariae and P. falciparum, and the staff administered oral quinine and doxycycline. Unfortunately, it was too late. Twelve days after admission, he died of multiorgan system failure and cardiac arrest at age 43. Mixed-species malaria infections are common but often not recognized.

As each generation of parasites matures and red blood cells rupture, the person develops a high fever and chills. In some cases, the malarial parasites also invade the brain or other organs. Cerebral malaria is fatal in about 20 percent of children. Those who survive repeated malarial infections acquire natural immunity by about age 10, but many suffer permanent brain damage, impaired vision, ruptured spleen, or damage to the heart, kidneys, or liver. Once nearly worldwide, malaria has been eliminated or controlled in most developed countries. It remains a major problem in the tropics and some subtropical areas, including subSaharan Africa, southeast Asia, Central America, and the Amazon region of South America. Malaria has essentially been eliminated from the United States, despite a few endemic cases as recently as 2003. Travelers to endemic areas may return with malaria (Case Study 2-3).

Who Is at Risk?

People are not at significant risk if they stay in a region where malaria does not occur. Global climate change and migration may change the present geographic limits of malaria, thus increasing the exposed population (Chapter 6). At present, about one-third of the global population is at risk. Even those with protective genes (such as sickle cell trait or thalassemia) can contract malaria, but the number of parasites in the blood usually stays low and the symptoms do not become severe. Africans with a gene called DARC have partial resistance to malaria but are at increased risk for HIV. Blood group O may confer some protection against malaria, as does a common genetic disorder called glucose6-phosphate dehydrogenase deficiency (G6PD). People with acquired resistance to malaria can tolerate the infection, but they are not fully immune either. An iron-rich diet or iron supplementation in children may increase susceptibility to malaria, but general malnutrition is also said to be a risk factor. Malaria is more likely to be severe or fatal in people who have other diseases, such as HIV, tuberculosis, dengue fever, or yellow fever. In some countries, hospital patients and transfusion recipients are at high risk for malaria. Accidental transmission by blood transfusion is fairly common where malaria is endemic and blood bank screening is inadequate.

The Numbers Every year, 400 to 500 million people contract malaria, and 1 to 2 million die as a result. An estimated 90 percent of these cases are in sub-Saharan Africa. Worldwide, about 20 percent of all childhood deaths result from malaria. On average, a child dies from this disease every 30 seconds. Sources



vary regarding the actual number of deaths, because many malaria victims also have other diseases such as yellow fever or tuberculosis. Also, children who die from malaria often succumb to one of its effects (such as anemia), which might be recorded as the proximate cause of death instead. Critics of global warming projections recently claimed that the largest malaria epidemic in history took place in Siberia during the 1920s and 1930s, with an estimated total of 13 million cases and 600,000 deaths over a 10-year period. These people concluded that malaria is not associated with hot climates and therefore will not expand its range if the Earth grows warmer. But this reasoning reflects a misunderstanding of the word “epidemic.” Even if the Siberian epidemic were the largest in history—which it wasn’t—malaria would still be a tropical disease, for the simple reason that the vast majority of cases occur in the tropics. An epidemic does not mean a large number of cases of a disease; it means a larger number than usual. Ethiopia, for example, normally has about 6 million cases of malaria every year. Those cases do not represent an epidemic, because they are normal for the region. But in 2003, the number of cases in Ethiopia jumped to about 12 million, and that was an epidemic.

History Scientists estimate that malaria has killed more people than any other disease in the history of the world—perhaps as many as half of all humans who have ever lived. Today, malaria is not only a deadly disease in its own right, but also a factor that has contributed to the AIDS epidemic in Africa, as discussed above. One of the oldest malaria treatments was a crude form of quinine obtained from the bark of South American evergreen trees in the genus Cinchona. This drug was called “the Jesuit powder” because missionary priests were among the first Europeans to recognize its value. Not everyone accepted this cure; Oliver Cromwell, Lord Protector of England, Scotland, and Ireland, contracted malaria in the marshes of Kent in his native England, but he refused treatment on religious grounds and died of the disease in 1658. George Washington had his first malaria attack in Virginia in 1749, with recurrences in 1752, 1761, 1784, and 1798. Theodore Roosevelt caught malaria in Brazil in 1914, and John F. Kennedy had it while stationed in the South Pacific during World War II. Other U.S. presidents who survived malaria include James Monroe, Andrew Jackson, Abraham Lincoln, Ulysses S. Grant, and James A. Garfield. Although malaria is primarily a tropical disease nowadays, the United States had millions of cases during the 1930s. The incidence diminished sharply by the 1940s, possibly as a result of New Deal malaria control projects or the depopulation of the rural South, where malaria was once prevalent. But malaria was already on the decline by 1928, before the New Deal or the use of DDT, thanks to a higher living standard that enabled people to live in houses with window screens. Without an infected host population, the disease tends to disappear.

Prevention and Treatment In 2009, researchers announced a major milestone in the age-old battle against malaria. An experimental vaccine developed by GlaxoSmithKline was more than 50 percent effective in preventing malaria in infants and toddlers in Kenya and Tanzania. If further testing is successful, the company may seek marketing approval in 2011, thus bringing the world one step closer to the United Nations’ goal of eliminating malaria (reducing the incidence to near zero) by 2015 and eradicating it altogether in the long term, perhaps by 2030.



Meanwhile, until a vaccine becomes available, the most effective preventive measures are also some of the oldest: wear protective clothing and mosquito repellent, avoid visiting endemic areas during the malaria season—unless, of course, you live there—and stay inside a screened building at night, preferably with a bed net. Taking antimalarial drugs (such as chloroquine or mefloquine) can reduce the probability of contracting malaria. But these drugs often have unpleasant side effects, such as nausea and depression, and they are not 100 percent effective. Since protozoan cells have a nucleus and chromosomes similar to those of higher animals, the drugs that kill protozoans tend to make people sick too. Also, some malarial parasites have become drug-resistant, like many other pathogens. Vendors of diluted antimalarial drugs have contributed to this problem by promoting the evolution of resistance without curing the disease. Antimalarial drugs are also expensive, and the cost of treatment is a major problem in most countries where malaria is endemic. In 2008, researchers reported progress in developing a method for inexpensive mass production of a phosphonate antimalarial compound. This process will help governments and individuals afford these drugs, but hopefully the new vaccine will soon render them redundant. The other way to prevent malaria is by vector control, usually involving elimination or management of standing water combined with Case Study 2-4: Malaria in Mauritius pesticide spraying (Case Study 2-4). As of 2009, The island nation of Mauritius is located in the controversy regarding the pesticide DDT has the southern Indian Ocean east of raged for more than 50 years. In 1972, the U.S. Madagascar, where conditions are favorgovernment outlawed DDT because of its harmable for malaria, yet the incidence of ful effects on wildlife, and many other nations malaria is very low. The reasons are rooted followed suit. Some people now claim that the in the history of the island. Neither humans removal of DDT from the arsenal sacrificed milnor malaria vectors (anopheline mosquilions of human lives in the name of environmentoes) were present on Mauritius until the mid-1700s, because cyclones made the tal protection; others point out that DDT was not island unsuitable for colonization. After working that well anyway, because some mosGreat Britain gained control of Mauritius quito populations had already acquired resisin 1810, sugar cane plantations and irrigatance before the chemical was banned. This tion canals replaced most of the original debate will most likely continue when malaria is forest. The human population increased to only a bad memory. At present, DDT is used on about 300,000, malaria vectors arrived on a limited basis for indoor spraying in some areas. ships from Africa, and a series of outbreaks followed. Between 1866 and 1868, about 10 percent of the population died of malaria. Survivors had partial immunity, but malaria was endemic on Mauritius for the next century. During World War II, British forces on the island started a vector control program that continued after the war. In 1973, the World Health Organization (WHO) declared Mauritius free of malaria, but four factors led to a resurgence between 1975 and 1984: standing water from a cyclone, new houses with flat roofs, infected migrant workers, and general complacence. The government redoubled its efforts, and the island has been free of indigenous malaria since 1996.

Popular Culture According to folklorists, people in Ghana believe that malaria is the result of working too hard in hot weather. In Gambia, there is a widespread belief that malaria results from drinking sour milk during the rainy season. In Togo, malaria is said to result from eating too much red palm oil. Others attribute the disease to witchcraft. In a 2005 study of mothers in Nigeria, 85 percent insisted that there was no connection between malaria and mosquitoes. These traditions are no more foolish than the nineteenthcentury European belief that malaria was the



result of bad air from swamps. But humans and malaria have coexisted in Africa for hundreds of thousands of years, and most Africans must have noticed the association with mosquitoes. Perhaps they know, but prefer not to tell; more than one folklorist has failed to recognize when someone was pulling his or her leg. Or perhaps it’s simply easier to attribute a disease to something controllable, such as food or work habits. Whatever the explanation, traditional beliefs persist in rural areas and may interfere with the acceptance of medical treatment. The 1985 motion picture Out of Africa devotes exactly five words to the subject of malaria: “My water’s gone black, Denys.” (This is a reference to blackwater fever, a late stage of malaria in which hemoglobin appears in the urine.) Mary Medearis’s 1942 novel Big Doc’s Girl is set in rural Arkansas during the Great Depression, where the title character takes on the state political establishment and a powerful real estate developer to fight a malaria epidemic. In North America, crushed leaves of the American beautyberry plant (Callicarpa americana) are a traditional folk remedy to repel mosquitoes. Recent studies show that this plant actually works. Other alleged remedies include black oak tea, garlic, white bryony root, peach, cow urine, dogwood, willow bark, and poplar bark. A popular malaria treatment in Thailand is a grass called ya ka (Imperata cylindrica) steeped in water. Known as cogon grass in English, it also grows in eastern and southern Africa, Indonesia, and Australia. In Togo, people reportedly make a tea called “malaria drink” from citronelle, ginger, and pineapple rinds to bring on sweating. West Africans reportedly use a bitter tea of neem leaves. Traditional Chinese remedies for malaria include concoctions of tang-shen (Campanumaea sp.), skullcap (Scutellaria baicalensis), Chinese quinine (Dichroa febrifuga), Chinese knotweed (Polygonum multiflorum), or magnolia (Magnolia officinalis), with the addition of toasted tortoise shell and peach kernels for chronic cases. At least one of these plants, Chinese quinine, contains an effective antimalarial compound. The side effects of antimalarial drugs are well documented in the medical literature. Depending on the drug, reported symptoms range from severe headache, upset stomach, and depression to nightmares, seizures, and violent behavior. Yet in every war since Vietnam, military personnel stationed in the tropics have been criticized for refusing to take their antimalarial medication due to unwarranted fears of side effects. In other words, there is an urban legend to the effect that the side effects of antimalarial drugs are nothing but an urban legend.

The Future The complete eradication of malaria will rank among the greatest of human achievements. When that day comes, the world should place all wars on hold, have a huge party, and make sure every colonist on Mars has been vaccinated. Chapter 6 discusses the potential effects of future climate change on malaria and several other diseases.

References and Recommended Reading AlKadi, H. O. “Antimalarial Drug Toxicity: a Review.” Chemotherapy, Vol. 53, 2007, pp. 385–391. Altman, L. K. “Diagnosis Was Malaria, but Experts Disagreed on the Source.” New York Times, 9 November 1999. “Anti-malarial Tablets Often Fake in Asia.” United Press International, 13 February 2008. Black, J., et al. “Mixed Infections with Plasmodium falciparum and P. malariae and Fever in Malaria.” Lancet, Vol. 343, 1994, p. 1095.



Bryson, D. “African Researchers Plan Malaria Vaccine Trial.” Associated Press, 10 November 2008. Campbell, C. C. “Malaria Control—Addressing Challenges to Ambitious Goals.” New England Journal of Medicine, Vol. 361, 2009, pp. 522–523. “CDC Allowed to Give Artesunate for Malaria.” Science Online, 4 August 2007. Chowdhury, K., and O. Bagasra. “An Edible Vaccine for Malaria Using Transgenic Tomatoes of Varying Sizes, Shapes and Colors to Carry Different Antigens.” Medical Hypotheses, Vol. 68, 2007, pp. 22–30. Cohen, S. “Immunity to Malaria.” Proceedings of the Royal Society of London, Series B, Biological Sciences, Vol. 203, 1979, pp. 323–345. Collins, W. E., and G. M. Jeffery. “Plasmodium malariae: Parasite and Disease.” Clinical Microbiology Reviews, Vol. 20, 2007, pp. 579–592. Connor, S., and M. Thomson. “Epidemic Malaria: Preparing for the Unexpected.” Science and Development Network, 1 November 2005. Cox-Singh, J., et al. 2008. “Plasmodium knowlesi Malaria in Humans Is Widely Distributed and Potentially Life Threatening.” Clinical Infectious Diseases, Vol. 46, 2008, pp. 165–171. Cox-Singh, J., and B. Singh. “Knowlesi Malaria: Newly Emergent and of Public Health Importance?” Trends in Parasitology, Vol. 24, 2008, pp. 406–410. “DDT Resistance Protein Found in Mosquitoes.” United Press International, 17 June 2008. Egan, T. J., and C. H. Kaschula. “Strategies to Reverse Drug Resistance in Malaria.” Current Opinion in Infectious Disease, Vol. 20, 2008, pp. 598–604. Filler, S. J., et al. “Locally Acquired Mosquito-Transmitted Malaria: A Guide for Investigations in the United States.” Morbidity and Mortality Weekly Report, 8 September 2006. “Gates Unleashes Mosquitoes at Tech Conference.” Associated Press, 6 February 2009. Greenwood, B. M., et al. “Malaria: Progress, Perils, and Prospects for Eradication.” Journal of Clinical Investigation, Vol. 188, 2008, pp. 1266–1276. Humphreys, M. “Water Won’t Run Uphill: The New Deal and Malaria Control in the American South, 1933–1940.” Parasitologia, Vol. 40, 1998, pp. 183–191. Hyde, J. E. “Drug-Resistant Malaria—An Insight.” FEBS Journal, Vol. 274, 2007, pp. 4688–4698. Ibidapo, C. A. “Perception of Causes of Malaria and Treatment-Seeking Behaviour of Nursing Mothers in a Rural Community.” Australian Journal of Public Health, Vol. 13, 2005, pp. 214–218. Jamieson, A., et al. 2006. Malaria: A Traveller’s Guide. Cape Town: Struik Publishers. Katz, T. M., et al. “Insect Repellents: Historical Perspectives and New Developments.” Journal of the American Academy of Dermatology, Vol. 58, 2008, pp. 8865–8871. Kitchen, A. D., and P. L. Chiodini. “Malaria and Blood Transfusion.” Vox Sanguinis, Vol. 90, 2006, pp. 77–84. Langhorne, J., et al. “Immunity to Malaria: More Questions than Answers.” Nature Immunology, Vol. 9, 2008, pp. 725–732. Lewison, G., and D. Srivastava. “Malaria Research, 1980–2004, and the Burden of Disease.” Acta Tropica, Vol. 106, 2008, pp. 96–103. MacArthur, J. R., et al. “Probable Locally Acquired Mosquito-Transmitted Malaria in Georgia, 1999.” Clinical Infectious Diseases, Vol. 32, 2001, pp. E124–E128. Mali, S., et al. “Malaria Surveillance—United States, 2006.” Morbidity and Mortality Weekly Report, Vol. 57, 2008, pp. 24–39. McKenzie, F. E., et al. “Strain Theory of Malaria: The First 50 Years.” Advances in Parasitology, Vol. 66, 2008, pp. 1–46. Mishra, S. K., and Mohanty, S. “Problems in Management of Severe Malaria.” Internet Journal of Tropical Medicine, Vol. 1, 2003, No. 1. Murdock, D. “DDT Key to Third World’s Winning War on Malaria.” Human Events, 14 May 2001. Nano, S. “Malaria Vaccine Shows Promise in Africa Tests.” Associated Press, 8 December 2008. Oppenheimer, S. “Comments on Background Papers Related to Iron, Folic Acid, Malaria and other Infections.” Food and Nutrition Bulletin, Vol. 28 (4 Suppl.), 2007, pp. S550–S559. O’Shaughnessy, P. T. “Parachuting Cats and Crushed Eggs: the Controversy over the Use of DDT to Control Malaria.” American Journal of Public Health, 17 September 2008. RBM (Roll Back Malaria) Partnership. “Global Roadmap to End Malaria Launched at UN Summit.” Press Release, 25 September 2008.



Ringwald, P. “Current Antimalarial Drugs: Resistance and New Strategies.” Bulletin de l’Académie Nationale de Médecin, Vol. 191, 2007, pp. 1273–1284. “Russia in Grip of Malaria Wave.” Universal Service, 4 August 1923. Skarbinski, J., et al. “Malaria Surveillance—United States, 2004.” Morbidity and Mortality Weekly Report, Vol. 55, 2006, pp. 23–37. “Study May Cut Malaria Treatment Costs.” United Press International, 1 October 2008. Thwing, J., et al. “Malaria Surveillance—United States, 2005.” Morbidity and Mortality Weekly Report, Vol. 56, 2007, pp. 23–40. Tripathy, V., and B. M. Reddy. 2007. “Present Status of Understanding on the G6PD Deficiency and Natural Selection.” Journal of Postgraduate Medicine, Vol. 53, 2007, pp. 193–202. United Nations. “World Leaders Commit Record Billions to Tackle Malaria.” Press Release, 25 September 2008. U.S. Centers for Disease Control and Prevention. “Treatment Guidelines: Treatment of Malaria (Guidelines for Clinicians).” March 2007. Walther, B., and M. Walther. “What Does It Take to Control Malaria?” Annals of Tropical Medicine and Parasitology, Vol. 101, 2007, pp. 657–672. White, N. J. 2008. “Qinghaosu (Artemisinin): The Price of Success.” Science, Vol. 320, 2008, pp. 330–334.

TUBERCULOSIS Summary of Threat Tuberculosis (TB) is an airborne bacterial disease that affects the lungs or other organs. Although preventable and curable, TB kills about 2 million people every year worldwide—more than any other single infectious agent. As of 2009, available vaccines are only partially effective, and some TB strains have become resistant to antibiotic treatment. HIV infection and malnutrition are major risk factors for TB. Other Names Tuberculosis is commonly called TB. Older names include consumption (“con” for short), phthisis, bacillary phthisis, phthisis pulmonalis, king’s evil, wasting disease, hectic fever, buck Irish, Pott’s disease, Koch’s disease, cachexia, and white plague. Specific forms of TB were called tabes mesenterica, lupus vulgaris, gibbus, fungous arthritis, or scrofula when the disease affected the abdominal lymph nodes, skin, spine, joints, or neck, respectively. The terms miliary tuberculosis and disseminated tuberculosis refer to TB that has invaded the circulatory system. A modern slang name for tuberculosis is “Victorian novel disease,” an allusion to its popularity as a plot device among fiction writers of that era. Primary tuberculosis is a person’s first infection with TB, usually in the lung; secondary tuberculosis means reinfection or reactivation of a dormant infection. The word “lunger” formerly meant a person with tuberculosis, but in modern slang the same word means a large wad of spit. Inelegant derivatives (according to some sources) include the slang words “looger” and “loogie.” TB has names in every language: kekkaku in Japanese, shachepheth in Hebrew, eitinn in Irish Gaelic, gorley shymlee in Manx Gaelic, and lugnasjúka in Faeroese. Description The word “tuberculosis” often conjures up an image of someone like the famous Doc Holliday, a thin person with interesting cheekbones who occasionally coughs blood into a handkerchief. In



Figure 2.5 Scanning electron micrograph showing Mycobacterium tuberculosis bacteria, which cause tuberculosis in humans. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

fact, tuberculosis takes many forms. Pulmonary (lung) tuberculosis is the most common, but TB can also affect the brain, lymph nodes, or other parts of the body (see Other Names). Many infected people are unaware that they have tuberculosis, because the disease often becomes latent for years before symptoms develop. An estimated one-third of the human population is infected with TB, and about 10 percent of those with healthy immune systems will eventually develop clinical disease. People who are HIV-positive are at even higher risk. In most of the world, the principal agent of human TB is a bacterium with the scientific name Mycobacterium tuberculosis (Figure 2.5). Several related species can also cause TB, particularly in persons with compromised immune systems. Transmission is usually by airborne droplet. Before the routine pasteurization of dairy products, people often developed scrofula or other forms of TB after drinking milk that was contaminated with the agent of bovine tuberculosis (Mycobacterium bovis).

Who Is at Risk? Tuberculosis is a re-emerging disease in the industrialized world, where it was on the decline until about 1985. Its recent resurgence is related to the spread of HIV (a major risk factor) and to immigration from Third World countries with a high prevalence of TB. As of 2009, immigrants to the United States from Mexico are three times more likely to have tuberculosis than the general U.S. population. There is an urgent need for better treatment programs to serve the needs of this immigrant group and prevent the disease from spreading. In addition to HIV, known risk factors for TB include alcoholism, malnutrition, smoking, air pollution, diabetes, and low serum vitamin D levels. Crowding also increases risk, because the



disease is airborne and spread by coughing. Studies suggest that African American, Hispanic, and Native American populations are more likely than others in the United States to develop TB. Certain occupational groups are at risk, such as hospital employees who work with TB patients or HIV-positive patients. The reverse can also happen; in 2008, a hospital worker with TB exposed an estimated 960 infants to the disease. Employees and residents of prisons, long-term care facilities, and homeless shelters also are at risk for TB. In at least two reported cases, a person with tuberculosis transmitted the disease to a group of friends while smoking marijuana in a shared bong or by “hotboxing” (smoking and exhaling inside a closed car).

The Numbers Tuberculosis kills more people worldwide each year than any other single infectious agent. Recent estimates range from 1.5 million to 3 million deaths per year, depending on who is counting. People with AIDS often contract TB (and other diseases such as malaria), and the recorded cause of death may not be accurate. During the first decade of the new millennium, about 9 million new cases of active TB appeared every year. About 95 percent of such patients are curable if they have access to treatment and are willing to cooperate, but about 5 percent have extensively drug-resistant tuberculosis (XDR-TB), which is essentially untreatable. In the United States, the cost of hospitalization for one XDR-TB patient averages about $483,000. Since XDR-TB does not respond to available antibiotics, these patients eventually die of the disease.

History Scientists have found traces of the TB bacterium in the remains of a South American woman who died some 500 years before Columbus reached the New World, a fact suggesting that the disease already had a worldwide distribution. Studies of ancient Egyptian mummies found TB in about one-third of them—the same as the prevalence in today’s human population. But tuberculosis appears to be even older than that. In 2007, anthropologists found evidence of a form of TB called tubercular meningitis in a 500,000-year-old human (Homo erectus) fossil from Turkey. It is possible that TB was originally a zoonosis found in wild ancestors of modern cattle and became a human disease soon after our ancestors began hunting and dismembering these animals. The public health impact of tuberculosis has long challenged human ingenuity. In the Old West, for example, bartenders deployed the latest medical advances to limit the spread of TB. Since it would be impolite to ask customers to refrain from spitting indoors, public spittoons were partially filled with an antiseptic such as carbolic acid. U.S. President Theodore Roosevelt recognized the association between tuberculosis and the conditions of poverty and crowding that many new immigrants encountered on their arrival in this country, but his proposed solution was harsh by today’s standards. In 1916, he wrote: If I could I would have the kind of restriction which would not allow any immigrant to come here unless I was content that his grandchildren would be fellow-citizens of my grandchildren. They will not be so if he lives in a boarding house at $2.50 per month with ten other boarders and contracts tuberculosis and contributes to the next generation a body of citizens inferior not only morally and spiritually but also physically.1 1. “A Roosevelt Idea Made in Germany” (New York Times, 2 February 1916).



No sentient being nowadays would call immigrants morally and spiritually inferior as a result of poverty or tuberculosis. Yet it is a statistical fact that people arriving in the United States from other countries account for the majority of active TB cases, and a solution better than rhetoric must be found. Recovering from this disease requires more than pluck and determination. It requires medical treatment, an increasingly unaffordable luxury for longtime residents and immigrants alike. During the first half of the twentieth century, the incidence of tuberculosis in the United States fell steadily, and many doctors were confident that this ancient enemy was on the run. Yet a cautious 1948 editorial predicted that TB might not yield so easily: On numerous occasions in the past, persons became over-enthusiastic and launched slogans such as “No Tuberculosis by 1920”; “No Tuberculosis by 1960”; “No Tuberculosis by the Year 2000”; “No Tuberculosis In Our Time,” etc., etc. Obviously those who prepared and publicized such slogans had not carefully analyzed the situation. . . . Even if all infection were to stop today, tuberculosis could not possibly be eradicated by the year 2000.2

Prevention and Treatment Many employers require regular tuberculin skin tests or chest X-rays. If more people would voluntarily request TB testing, many lives might be saved. Treatment of latent tuberculosis infection with drugs such as isoniazid helps to prevent progression to active disease. Nor is active TB an automatic death sentence. If it is detected early, and if the patient cooperates fully with treatment, full recovery is possible in about 95 percent of cases. Treatment usually lasts several months and requires a combination of several antimicrobial drugs (usually isoniazid, rifampin, and pyrazinamide) with frequent testing of sputum. A 2009 study found that these drugs are more effective at higher doses. Like many other diseases, however, tuberculosis has given rise to drug-resistant strains that are difficult to treat: the increasingly prevalent multidrug-resistant TB (MDR-TB), found in up to 36 percent of previously treated TB patients, and extensively drug-resistant TB (XDR-TB), which accounts for about 5 percent of cases. Combinations of second-line drugs such as amikacin, kanamycin, capreomycin, or the fluoroquinolone wide-spectrum antibiotics, often are effective against resistant strains. In 2008, scientists at Rutgers University announced the discovery of a new class of antibiotics that might help combat drug-resistant TB and other diseases. The BCG (Bacille Calmette-Guérin) tuberculosis vaccine has been available since 1921, but it is seldom used in the United States because of concerns regarding its efficacy. It can prevent disseminated TB and TB meningitis in children, but otherwise the results of testing have been inconsistent and appear to vary by population and latitude, with little or no protective effect near the equator. As of 2009, research was in progress to develop new TB vaccines or adjuvants. In some cases, recovery from TB requires surgery as well as antibiotic treatment. In 2008, doctors in Europe successfully replaced a former TB patient’s damaged windpipe by growing a new one from her own stem cells. Doctors may also use surgery to remove part of a damaged lung in cases of drug-resistant TB. As a last resort, governments may isolate tuberculosis patients to protect the general population from infection. In 2008, the press reported that a South African hospital isolated TB patients by means of razor wire and armed guards. Although such policies might sound extreme, public health officials have limited options when dealing with noncompliant patients 2. “Tuberculosis Eradication Being Achieved” (Chest, Vol. 14, 1948, pp. 292–293).


or those with extensively drug-resistant tuberculosis. In 2007, more than one TB patient made headlines in the United States by ignoring doctors’ orders and exposing others to the disease (Case Study 2-5).

Popular Culture


Case Study 2-5: An Airplane Passenger In the summer of 2007, the news media reported the case of a Georgia attorney with multidrug-resistant tuberculosis (MDR-TB) who allegedly ignored his doctor's advice and flew to Greece to get married. When he and his wife returned to the United States, the CDC thought he had a more dangerous form of the disease, known as extensively drug-resistant TB (XDR-TB) and took him into custody to protect the public. Soon after his release, he had surgery to remove diseased lung tissue. Public reaction seemed divided between (1) outrage at the government for restricting this man’s freedom and (2) outrage at the government for allowing him to fly in the first place. A similar incident in 2006 received less publicity, when an Arizona TB patient was taken into custody. And in October 2007, the Washington Times reported that a Mexican national with XDR-TB had recently crossed the U.S. border 76 times and had taken multiple domestic flights. Given the apparent difficulty of enforcing public health laws or identifying passengers, the simplest solution might be to have all airline passengers wear protective masks, whether infected or not.

In the old days before antibiotics, TB victims tended to be pale and thin, and they were often seen with blood on their faces. The explanation was obvious: they must be vampires! Perhaps the most famous example was Mercy Brown, who died of TB in Exeter, Rhode Island, in 1892 at age 20. Her mother and two sisters had previously died of the same disease, and her older brother had also contracted it. For some reason, the neighbors decided that one member of the Brown family must be a vampire who was attacking the others. So they opened Mercy’s above-ground crypt, two months after her death, and found the body relatively fresh. Instead of attributing its condition to the cold winter weather, they identified her as the vampire, and insisted on removing and burning her heart. They even made her brother drink some of the ashes for good measure, but he died of TB a few months later. (This appears to be a true story, except for the part about Mercy Brown being a vampire.) Tuberculosis is a theme in many works of art and literature. In the Puccini opera La Bohème, the heroine is a beautiful young seamstress named Mimi who dies of TB. In the 1936 motion picture Camille and the Verdi opera La Traviata, the heroine is a beautiful young courtesan who dies of TB. And then there was Fantine in Les Miserables, and Beth in Little Women, and Helen in Jane Eyre. Thomas Mann’s 1924 novel The Magic Mountain takes place in a tuberculosis sanitarium. A more recent example is Nicole Kidman’s character Satine in the 2001 motion picture Moulin Rouge. A gritty treatment of TB appears in Upton Sinclair’s 1906 novel The Jungle, in which meatpackers suffer most unromantically from this disease. John le Carré’s 2001 novel The Constant Gardener deals with the testing of tuberculosis drugs on unaware subjects in Africa. And in the 1964 memoir A Moveable Feast, Ernest Hemingway notes that prostitutes in Kansas City believed that swallowing semen would cure tuberculosis. North American and European folk remedies for TB include deer’s tongue (a plant), elder, sagebrush, red clover, sanicle, cocklebur, creosote bush, or pine resin; a mixture of lemon, honey, and flaxseed; mistletoe, St. John’s wort, blackberry, garlic, tobacco, eggs, ginseng, valerian, elecampane, logwood (Haematoxylon campechianum), yellow dock, whortle berries (Vaccinium arboreum), hellebore (Veratrum viride), wild lettuce (Lactuca canadensis), liverwort,



Case Study 2-6: Umckaloabo Don’t ask us how to pronounce this word, but it is a blend of two equally difficult Zulu words that mean “lung disease” and “breast pain.” Umckaloabo is an herbal medicine that African healers have used for generations to treat tuberculosis. The principal ingredient is the root of Pelargonium, a relative of the garden geranium. Every culture has its traditional remedies, but this one has gained worldwide fame thanks to the marketing genius of an Englishman named Charles Henry Stevens (1880–1942). Diagnosed with TB in 1897, Stevens moved to South Africa on his doctor's advice and was allegedly cured by a local medicine man. After the Boer War, he founded a company to sell the wonderful root. Despite decades of insults from an unsympathetic medical establishment, Stevens became a wealthy man and eventually died from an infected scratch on his leg. The story of Umckaloabo did not end there; a Swiss physician heard about the remedy and became its next champion. He reported some anecdotal success in treating TB patients, but he was unable to conduct clinical trials because Stevens never disclosed the identity of the plant. That mystery was solved in 1977, when a laboratory identified a sample as Pelargonium. As of 2005, the product is popular in Germany and other European countries, but nobody has yet figured out whether it really works or not.

mullein, nettle leaf tea, juniper tea, buttercup, or dew shaken from the flowers of chamomile; warm milk from a red cow or from a goat of any color; dew from a manure pile; the fat of a turtle, alligator, or rattlesnake; pickled rattlesnake skin, small frogs, cooked raccoon, or blood from the tail of a cat without a white hair; bogbean or buckbean (Menyanthes trifoliata); soup made from a black dog, or the hind limb of any dog; tea made by boiling potato peelings; walking to a spot where four winds meet; being bitten by a rattlesnake; wearing a cat skin on the chest, or allowing a cat to sleep on the bed; inhaling fumes from a cattle shed or horse stall, or those of a skunk, or the air of pine woods; or applying a salve of twinleaf root. Traditional Chinese herbal remedies for pulmonary tuberculosis include concoctions of fresh marlberry (Ardisia japonica), figwort (Scrophularia sp.), or fritillary (Fritillaria verticillata), or powdered roots of Indian madder (Rubia cordifolia), rhubarb (Rheum rhabarbarum), oriental arborvitae (Thuja orientalis), or Chinese ground orchid (Bletilla sp.) mixed with juice of crushed radish. See also Case Study 2-6. The Future

As of 2009, WHO was midway through its Global Plan to Stop TB, with the goal of reducing new cases and deaths by 50 percent by the year 2015 and eliminating the disease (reducing its incidence to one case per million population) by 2050. Key elements of this plan include making treatment more accessible and affordable, and promoting research to develop new TB tests and drugs. Unfortunately, the consensus appears to be that these goals are not yet feasible. Elimination of TB will most likely require an effective vaccine, reduction of risk factors, and more rapid progress in improving healthcare for low-income people.

References and Recommended Reading Al-Jahdali, H., et al. “Tuberculosis in Association with Travel.” International Journal of Antimicrobial Agents, Vol. 21, 2003, pp. 125–130. Bloom, B. R., and P. M. Small. “The Evolving Relation Between Humans and Mycobacterium tuberculosis.” New England Journal of Medicine, Vol. 338, 1998, pp. 677–678. Blue, L. “A New Class of Antibiotics Could Offer Hope Against TB.” Time, 17 October 2008. Brosch, R., and V. Vincent. “Cutting-Edge Science and the Future of Tuberculosis Control.” Bulletin of the World Health Organization, Vol. 85, 2007, pp. 410–412.



Budha, N. R., et al. “Biopharmaceutics, Pharmacokinetics and Pharmacodynamics of Antituberculosis Drugs.” Current Medicinal Chemistry, Vol. 15, 2008, pp. 809–825. Burzynski, J., and W. Schluger. “The Epidemiology of Tuberculosis in the United States.” Seminars in Respiratory and Critical Care Medicine, Vol. 29, 2008, pp. 492–498. Castro, K. G. “Tuberculosis Elimination in the United States: Why, How, and What Will It Take?” Kekkaku, Vol. 83, 2008, pp. 93–100. “Cincy Homeless Shelter Hit with TB.” Science Online, 5 May 2007. “Diabetes May Increase Risk of Developing TB.” Reuters, 15 July 2008. “Drug-Resistant TB Is 5 Percent of All TB.” United Press International, 26 February 2008. European Centre for Disease Prevention and Control. “Framework Action Plan to Fight Tuberculosis in the European Union.” Stockholm, February 2008. Fattorini, L., et al. “Extensively Drug-Resistant (XDR) Tuberculosis: An Old and New Threat.” Annali dell’Istituto Superiore di Sanità, Vol. 43, 2007, pp. 317–319. Fernandez, E. “960 Babies in TB Scare at Kaiser in S. F.” San Francisco Chronicle, 27 August 2008. Khan, K., et al. “Tuberculosis Infection in the United States: National Trends Over Three Decades.” American Journal of Respiratory and Critical Care Medicine, Vol. 177, 2008, pp. 455–460. Kilner, J. “Siberian Jail Is Champion in Fight against TB.” Reuters, 4 July 2008. Klein, A. “New Drug Targets May Fight Tuberculosis and Other Bacterial Infections in Novel Way.” Weill Cornell Medical College, press release, 27 December 2007. LoBue, P., et al. “Plan to Combat Extensively Drug-Resistant Tuberculosis: Recommendations of the Federal Tuberculosis Task Force.” Morbidity and Mortality Weekly Report, 12 February 2009. Lönnroth, K., and M. Raviglione. “Global Epidemiology of Tuberculosis: Prospects for Control.” Seminars in Respiratory and Critical Care Medicine, Vol. 29, 2008, pp. 481–491. Maâlej, S., et al. “Pulmonary Tuberculosis and Diabetes” [French]. Presse Medicale, 2 September 2008. Marks, S. M., et al. “Knowledge, Attitudes and Risk Perceptions about Tuberculosis: U.S. National Health Interview Survey.” International Journal of Tuberculosis and Lung Disease, Vol. 12, 2008, pp. 1261–1267. “Most Ancient Case of Tuberculosis Found in 500,000-Year-Old Human; Points to Modern Health Issues.” University of Texas at Austin, press release, 7 December 2007. Naidoo, R. “Surgery for Pulmonary Tuberculosis.” Current Opinion in Pulmonary Medicine, Vol. 14, 2008, pp. 254–259. Nnoaham, K. E., and A. Clarke. “Low Serum Vitamin D Levels and Tuberculosis: A Systematic Review and Meta-Analysis.” International Journal of Epidemiology, Vol. 37, 2008, pp. 113–119. Oeltmann, J. E., et al. “Tuberculosis Outbreak in Marijuana Users, Seattle, Washington, 2004.” Emerging Infectious Diseases, Vol. 12, 2006, pp. 1156–1159. Pieters, J. “Mycobacterium tuberculosis and the Macrophage: Maintaining a Balance.” Cell Host and Microbe, Vol. 3, 2008, pp. 399–407. Raviglione, M. C. “The New Stop TB Strategy and the Global Plan to Stop TB, 2006–2015.” Bulletin of the World Health Organization, Vol. 85, 2007, p. 327. Stevenson, C. R., et al. “Diabetes and the Risk of Tuberculosis: A Neglected Threat to Public Health?” Chronic Illness, Vol. 3, 2007, pp. 228–245. Storla, D. G., et al. “A Systematic Review of Delay in the Diagnosis and Treatment of Tuberculosis.” BMC Public Health, Vol. 8, 2008, p. 15. “TB Eradication in the U.S. by 2010 Unlikely: Survey.” Reuters Health, 5 February 2008. “TB on a Plane? Expect More of It, Experts Say.” Associated Press, 31 May 2007. “TB Patient Gets New Windpipe Made with Own Stem Cells.” Medical News Today, 19 November 2008. “Tuberculosis Found in Ancient Homo erectus.” Science Online, 7 December 2007. U.S. Centers for Disease Control and Prevention. “BCG Vaccine.” Fact Sheet, April 2006. Weinberg, E. D. “Iron Out-of-Balance: A Risk Factor for Acute and Chronic Diseases.” Hemoglobin, Vol. 32, 2008, pp. 117–122. Young, D. B., et al. “Confronting the Scientific Obstacles to Global Control of Tuberculosis.” Journal of Clinical Investigation, Vol. 118, 2008, pp. 1255–1265.



INFLUENZA Summary of Threat Influenza (flu) is an airborne viral disease that causes fever and respiratory illness, sometimes with complications such as pneumonia. About 1 million people die from influenza in a typical year, but large epidemics of certain flu strains have caused many more deaths. As of 2009, flu vaccines and antiviral drugs are only partially effective. Influenza affects not only humans, but also birds, pigs, and other animals.

Other Names The name “influenza” refers to the fact that medieval astronomers attributed disease epidemics to cosmic influences. English names for influenza include flu, grippe, and epidemic

Figure 2.6 Scanning electron micrograph showing influenza virus of the type that caused the 1918 pandemic. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



catarrhal fever. The nickname “panflu” for pandemic influenza also appears to be catching on. Words for flu in most other languages are cognates of the English words; for example, floo in Manx, grip in Turkish, and imfluwenza in Zulu. Outbreaks and subtypes of influenza tend to acquire nicknames. The 1918 pandemic (source unknown) was called the Spanish Flu, Spanish Lady, Naples Soldier, La Grippe Espagnole (French for “Spanish grippe”), or La Pesadilla (Spanish, “the nightmare”). Other names may refer to a host (swine flu, bird flu, chicken flu, avian influenza) or point of origin (Asian flu, London flu, Hong Kong flu, Johannesburg flu, Guangdong flu, New Caledonian flu, Panama flu, Sichuan flu, Shanghai flu, London flu, Kamamoto flu); a full catalog would exceed the scope of this book. The so-called “stomach flu” (viral gastroenteritis) is not related to influenza, although some flu strains may cause nausea or diarrhea in addition to the usual flu symptoms. (Likewise, despite its name, the bacterium Haemophilus influenzae is not the agent of influenza.) Antigenic subtypes of the influenza A virus (Figure 2.6) get their official names from the types of glycoproteins found on the surface of the virus (Figure 2.7). The letter H followed by a number identifies a glycoprotein called a hemagglutinin, and the letter N followed by a number identifies another glycoprotein called a neuraminidase. For example, H1N1 refers to a subtype

Figure 2.7 Diagram of Influenza A virion. Source: J. R. Callahan, Biological Hazards (Oryx Press, 2002).



with hemagglutinin 1 and neuraminidase 1. Influenza is also characterized by outbreak pattern: seasonal, pandemic, or sporadic.

Description Influenza A, a disease of humans and various domesticated and wild animals, is the type responsible for most human epidemics and all recorded pandemics. The media’s favorite flu viruses, such as H1N1 and H5N1, are subtypes of influenza A. Influenza B has caused some regional epidemics, and influenza C is usually limited to sporadic cases and small outbreaks. This discussion will focus on influenza A. Influenza usually starts abruptly, with a high fever, headache, and muscle pain. After a few days, these symptoms often subside, and the person develops a persistent dry cough, sore throat, and runny nose. The cough and general fatigue may last for weeks, and serious complications may develop, such as pneumonia or encephalitis (Chapter 3). Influenza is an example of a zoonosis—a disease that infects both humans and other species, in this case primarily birds and pigs. In the tropics, influenza A occurs throughout the year, but in temperate regions of both hemispheres, epidemics occur mainly in winter. These seasonal epidemics usually start in Asia, apparently because of farming practices that bring humans into close contact with millions of ducks, chickens, and pigs, which serve as a reservoir for the disease and as a de facto laboratory for the evolution of new strains. Worldwide flu epidemics, known as pandemics, also occur periodically (see History).

Who Is at Risk? Anyone can catch the flu, but for most people it is a mild disease with a very low death rate (usually less than 0.01 percent). The risk of bacterial pneumonia, or other serious complications of influenza, is usually higher if at least one of the following factors is present: age under 2 or over 65 , asthma or other chronic respiratory disease, diabetes, poor nutritional status, low-dose arsenic exposure, or a compromised immune system. Some forms of influenza are more virulent than others; in 2008, researchers estimated that the human case fatality rate of highly pathogenic avian influenza (Chapter 4) is somewhere between 14 percent and 33 percent. Healthcare workers and bartenders are often at high risk for influenza because of indoor exposure to people and their sputum. People who live or work in crowded conditions, those exposed to secondhand smoke, and those who use public transportation are also at increased risk for airborne diseases in general. Factors that reduce the probability of catching the flu include youth (for most strains), acquired immunity from previous exposure to the same subtype, having annual flu shots, wearing a protective mask and gloves in public, and avoiding all contact with other human beings or contaminated objects. Clearly, some of these precautions are more feasible than others. These risk factors refer to recent subtypes and epidemics. In the 1918 pandemic, however, a high proportion of those who died were military recruits and other young, healthy people. That discrepancy is one of several reasons why scientists believe that secondary or concurrent infections, such as TB and pneumonia, were largely responsible for the high death rate. As of 2009, it is unclear if youth is a risk factor for complications resulting from the H1N1 swine flu, or if older people simply have partial resistance because of prior exposure to a similar strain.



The Numbers In a typical year, 10 to 20 percent of U.S. residents contract influenza, and some 200,000 are hospitalized with complications of influenza. About 36,000 to 40,000 die, usually as the result of a secondary infection such as pneumonia. Worldwide, there are about 500,000 to 1 million flurelated deaths every year. In a pandemic year, these numbers change. The 1918 pandemic killed at least 40 to 50 million people, with some recent estimates running as high as 100 million. These numbers tend to dominate every discussion of influenza. The global population in 1918 was about 1.8 billion; in 2009, there were about 6.8 billion, including hundreds of millions with compromised immune systems, diabetes, or other chronic medical conditions that represent risk factors for influenza. As a result, some (not most) sources predict that the next influenza pandemic might kill as many as 1 billion people.

History Between the isolation of the influenza virus in 1933 and the advent of HIV in 1981, influenza was perhaps the focus of more intensive study than any other viral disease. There were two influenza pandemics during that interval, in 1957 and 1968. Sources do not agree on the exact number of past pandemics, since records are incomplete, but there have been at least nine since written records became available (Table 2.3). The H1N1 influenza outbreak of 2009 achieved pandemic status shortly before this book went to press. Note that the word “pandemic” refers to the numbers and distribution of cases, and does not necessarily imply a high death rate. The 1918 influenza pandemic changed the world in many ways, not all of them immediately apparent. For example, in April 1919, President Woodrow Wilson contracted influenza (perhaps complicated by encephalitis) while representing the United States at the Paris Peace Conference. He survived, but was unable to participate effectively in the conference. Without his input, the resulting treaty created economic hardship in postwar Germany that would soon favor the rise of a ruthless dictator.

Prevention and Treatment Preventive measures include avoidance and vaccination. Researchers prepare an influenza vaccine each year, based on the viral strains that appear to be circulating, but this approach Table 2.3 Influenza Pandemics Date


Estimated Deaths


1580 1729 1782 1830 1847 1889 1918 1957 1968

none (Europe) Russian Flu Blitz Catarrh China Flu none (Europe) Russian Flu Spanish Flu Asian Flu Hong Kong Flu

Unknown Unknown Unknown 1 to 2 million? 1% injections), in decreasing order of frequency, were irritability, fever (>101°F oral equivalent), diarrhea, fatigue/weakness, diminished appetite, and rhinitis.5

These symptoms last for hours or days, not for the rest of the person’s life, and they are not necessarily related to the vaccine. In clinical trials, a comparable percentage of subjects who take a placebo report similar symptoms. This controversy regarding the hepatitis B vaccine apparently started in the early 1990s, with scattered reports of neurological symptoms that developed within a few weeks or months after HBV vaccination. In 2001, a French court ordered a vaccine manufacturer to pay damages to two women who developed multiple sclerosis. A higher court overturned that judgment in 2004, and further studies have shown no connection to MS, but the public relations damage was done. About 1 in 600,000 hepatitis B shots does cause an allergic reaction called anaphylaxis, and the longterm consequences (if any) are unknown; but no one on record has died from this complication, which is clearly preferable to liver cancer or other known sequelae of hepatitis B. Prevention and Treatment Obvious preventive measures include avoidance of dirty needles, unprotected sex, or contact between open wounds and contaminated surfaces. Women should be tested for hepatitis B and C before having children. Again, however, not all cases of hepatitis reflect a careless lifestyle. Many 4. Association of American Physicians and Surgeons, letter to Cook County Board of Commissioners, 10 March 2004. 5. Merck & Co., Inc., product information, Recombivax HB Hepatitis B Vaccine, December 2007.



people become infected as the result of medical or dental accidents, or other circumstances they cannot prevent. The hepatitis B vaccine is safe for most people, unless they are allergic to baker’s yeast. According to some sources, however, this vaccine may be unavailable to many low-income adults and older children. Many other people seem unaware of the vaccine or avoid it because of concerns about side effects. There is also some evidence that exposure to shortwave ultraviolet light reduces the effectiveness of HBV vaccination. In 2005, researchers announced an experimental edible hepatitis B vaccine in a transgenic potato. This discovery may or may not improve the public image of the vaccination program, particularly if the potato must be eaten raw. As of 2009, there is no hepatitis C vaccine. Doctors sometimes treat both hepatitis B and hepatitis C with antiviral drugs (usually interferon and ribavirin), but drug-resistant mutant viruses have already begun to appear. These antiviral drugs can cause psychiatric side effects such as depression and anxiety. A 2008 study concluded that drinking large amounts of coffee may slow the progression of hepatitis C, but this finding is hard to evaluate. An alternative explanation for the data is that people whose livers are in bad shape might tend to reduce or underreport their coffee intake. Popular Culture Some researchers claim that an Indian plant called keezhanali (Phyllanthus amarus) is an effective treatment for hepatitis B, but others regard the evidence as inconclusive. In a 2001 study, for example, this herbal treatment reportedly cured 30 percent of cases within a month. But even without treatment, the majority of patients recover. Plutarch (A.D. 46–120) claimed that it was possible to cure hepatitis by having the patient look at a stone curlew, a European bird with large yellow eyes that supposedly drew out the disease. Other reported folk cures for hepatitis or jaundice include eating artichokes, spiders, head lice (live or boiled), sheep dung, tobacco, or extracts of at least 100 different wild plants, some of them poisonous; or wearing yellow clothes, copper coins, or a necklace of beets; or placing hard-boiled eggs in the armpits overnight, or urinating through a bored-out carrot. Traditional Chinese herbal remedies for infectious hepatitis include concoctions of wormwood (Artemesia capillaris), self-heal (Prunella vulgaris), azuki bean (Phaseolus angularis), crowdipper (Pinella ternata), three-leaf corydalis (Corydalis ternata), or nut grass (Cyperes rotundus). In 2005, the American Liver Foundation condemned the motion picture Bewitched because of a scene in which a woman discourages romantic overtures by claiming she has hepatitis C. The incident is reminiscent of a 1970s “Mary Worth” cartoon in which a young woman told an unwanted admirer that she was a mumps carrier. Politically correct or not, this strategy is probably as old as dating. In 1999, the TV show 20/20 did a segment “Who’s Calling the Shots?” about children and adults who developed arthritis or multiple sclerosis after receiving the hepatitis B vaccine. The program was somewhat misleading, because these disorders occur at the same frequency in people who have not had the vaccine. Opponents argue that babies rarely catch hepatitis B, so what’s the point of vaccinating them? Why not wait until they grow up, and let them decide? Aside from the obvious problems, children infected before age 6 are more likely to get chronic liver disease and liver cancer. Some children apparently get hepatitis B through ordinary household contacts with infected family members. The Future The world clearly needs a hepatitis C vaccine. Unless the healthcare establishment can gain the trust of the general public, however, this new vaccine (like the hepatitis B vaccine) may be



underutilized, and many children and adults at risk may go unprotected. Further study of the hepatitis B vaccine, and further investigation of opponents’ claims, might alleviate some concerns.

References and Recommended Reading “40 Die in Hepatitis-B Outbreak in Western Indian State.” Xinhua News Agency, 21 February 2009. Baldo, V., et al. “Epidemiology of HCV Infection.” Current Pharmaceutical Design, Vol. 14, 2008, pp. 1646–1654. Bereket-Yücel, S. “Risk of Hepatitis B Infections in Olympic Wrestling.” British Journal of Sports Medicine, Vol. 41, 2007, pp. 306–310. Blackard, J. T., and K. E. Sherman. “HCV/HIV Co-infection: Time to Re-evaluate the Role of HIV in the Liver?” Journal of Viral Hepatitis, Vol. 15, 2008, pp. 323–330. Brautbar, N., and N. Navizadeh. “Sewer Workers: Occupational Risk for Hepatitis C—Report of Two Cases and Review of Literature.” Archives of Environmental Health, Vol. 54, 1999, pp. 328–330. Brook, M. G. “Sexually Acquired Hepatitis.” Sexually Transmitted Infections, Vol. 78, 2002, pp. 235–240. Calabrese, L. H., et al. “Hepatitis B Virus (HBV) Reactivation with Immunosuppressive Therapy in Rheumatic Diseases: Assessment and Preventive Strategies.” Annals of the Rheumatic Diseases, Vol. 65, 2006, pp. 983–989. Cavalheiro, N. P. “Sexual Transmission of Hepatitis C.” Revista do Instituto de Medicina Tropical de São Paulo, Vol. 49, 2007, pp. 271–277. Craxi, A., et al. “Hepatitis C Virus (HCV) Infection: a Systemic Disease.” Molecular Aspects of Medicine, Vol. 29, 2008, pp. 85–95. de Carvalho, J. F., and Y. Shoenfield. “Status Epilepticus and Lymphocytic Pneumonitis Following Hepatitis B Vaccination.” European Journal of Internal Medicine, Vol. 19, 2008, pp. 383–385. De Sanjose, S., et al. “Hepatitis C and Non-Hodgkin Lymphoma among 4784 Cases and 6269 Controls from the International Lymphoma Epidemiology Consortium.” Clinical Gastroenterology and Hepatology, Vol. 6, 2008, pp. 451–458. Dowd, J. B., et al. “Early Origins of Health Disparities: Burden of Infection, Health, and Socioeconomic Status in U.S. Children.” Social Science and Medicine, 17 January 2009. Edelman, S., and J. Culora. “Doctor ‘Disease.’” New York Post, 17 June 2007. Ghoda, M. K., and R. A. Shah. “A Prospective Epidemiological Study to See if Mosquito Bite Could Be Responsible for Spread of Hepatitis B Virus Infection.” Tropical Gastroenterology, Vol. 26, 2005, pp. 29–30. Hatfield, G. 2004. Encyclopedia of Folk Medicine. Santa Barbara, CA: ABC-CLIO. “Hepatitis B Vaccine Not Linked to MS.” United Press International, 30 September 2008. Hsu, E. K., and K. F. Murray. “Hepatitis B and C in Children.” Nature Clinical Practice Gastroenterology and Hepatology, Vol. 5, 2008, pp. 311–320. “Infection Control Flaws Found at Most Nevada Clinics.” Associated Press, 10 March 2009. Jancin, B. “Sweat of Infected Patients May Contain Hepatitis C: Inapparent Parenteral Transmission.” OB/GYN News, 15 December 2003. Kamal, S. M. “Acute Hepatitis C: a Systematic Review.” American Journal of Gastroenterology, Vol. 103, 2008, pp. 1283–1297. Marshall, E. “A Shadow Falls on Hepatitis B Vaccination Effort.” Science, Vol. 281, 1998, pp. 630–631. Mauss, S., and H. Wedemeyer. “Treatment of Chronic Hepatitis B and the Implications of Viral Resistance to Therapy.” Expert Review of Anti-Infective Therapy, Vol. 6, 2008, pp. 191–199. Mikaeloff, Y., et al. “Hepatitis B Vaccination and the Risk of Childhood-Onset Multiple Sclerosis.” Archives of Pediatric and Adolescent Medicine, Vol. 161, 2007, pp. 1176–1182. Mikaeloff, Y., et al. “Hepatitis B Vaccine and the Risk of CNS Inflammatory Demyelination in Childhood.” Neurology, 8 October 2008. Missiha, S. B., et al. “Disease Progression in Chronic Hepatitis C: Modifiable and Nonmodifiable Factors.” Gastroenterology, Vol. 134, 2008, pp. 1699–1714. Nadler, J. P. “Multiple Sclerosis and Hepatitis B Vaccination.” Clinical Infectious Diseases, Vol. 17, 1993, pp. 928–929.



Nash, K. L., and G. J. Alexander. “The Case for Combination Antiviral Therapy for Chronic Hepatitis B Virus Infection.” Lancet Infectious Diseases, Vol. 8, 2008, pp. 444–448. “Ninth Las Vegas Hepatitis C Case Confirmed.” United Press International, 24 July 2008. Panella, H., et al. “Transmission of Hepatitis C Virus During Computed Tomography Scanning with Contrast.” Emerging Infectious Diseases, Vol. 14, 2008, pp. 333–336. Perez, C. M., et al. “Hepatitis C in Puerto Rico: a Time for Public Health Action.” Puerto Rico Health Sciences Journal, Vol. 26, 2007, pp. 395–400. “Police Hunt for Two-Day-Old Baby to Enforce Hepatitis Jab Order.” Agence France Presse, 22 August 2008. Ramirez, A. “Three NYC Hepatitis Cases Linked to M.D.” The New York Times, 15 June 2007. Rodriguez-Torres, M. “Latinos and Chronic Hepatitis C: A Singular Population.” Clinical Gastroenterology and Hepatology, Vol. 6, 2008, pp. 484–490. Rougé-Maillart, C. I., et al. “Recognition by French Courts of Compensation for Post-Vaccination Multiple Sclerosis: The Consequences with Regard to Expert Practice.” Medicine, Science and Law, Vol. 47, 2007, pp. 185–190. Saunders, J. C. “Neuropsychiatric Symptoms of Hepatitis C.” Issues in Mental Health Nursing, Vol. 29, 2008, pp. 209–220. Seifert, F., et al. “In Vivo Detection of Hepatitis C Virus (HCV) RNA in the Brain in a Case of Encephalitis: Evidence for HCV Neuroinvasion.” European Journal of Neurology, Vol. 15, 2008, pp. 214–218. Sharfstein, J. “Inadequate Hepatitis B Vaccination of Adolescents and Adults at an Urban Community Health Center.” Journal of the National Medical Association, Vol. 89, 1997, pp. 86–92. Sheikh, M. Y., et al. “Hepatitis C Virus Infection: Molecular Pathways to Metabolic Syndrome.” Hepatology, Vol. 47, 2008, pp. 2127–2133. Strickland, G. T., et al. “Hepatitis C Vaccine: Supply and Demand.” Lancet Infectious Diseases, Vol. 8, 2008, pp. 379–386. Thanavala, Y., et al. “Immunogenicity in Humans of an Edible Vaccine for Hepatitis B.” Proceedings of the National Academy of Sciences (USA), Vol. 102, 2005, pp. 3378–3382. Thompson, N. D., et al. “Nonhospital Health Care-Associated Hepatitis B and C Virus Transmission: United States, 1998–2008.” Annals of Internal Medicine, Vol. 150, 2009, pp. 33–39. Wasley, A., et al. “Surveillance for Acute Viral Hepatitis—United States, 2005.” Morbidity and Mortality Weekly Report Surveillance Summaries, Vol. 56, 2007, pp. 1–28. Weissenborn, K., et al. “Hepatitis C Virus Infection and the Brain.” Metabolic Brain Disease, 7 January 2009. Wise, M., et al. “Changing Trends in Hepatitis C–Related Mortality in the United States, 1995–2004.” Hepatology, Vol. 47, 2008, pp. 1128–1135. “Witnesses Quiet on Hepatitis C Outbreak.” United Press International, 30 September 2008.

This page intentionally left blank


Five More (and Complications)

My name is Legion, for we are many. —King James Bible, Mark 5:9

In 1924, when 16-year-old Calvin Coolidge Jr. (the president’s son) had an infected blister on his foot, the antibiotics that we take for granted today were unknown. The infection spread to his bloodstream, and in a few days he was dead. If the same thing happened in 1954 or 1974 instead of in 1924, an antibiotic such as penicillin might have quickly cured the problem. As early as the 1960s, however, doctors noticed that some infections were becoming unresponsive to antibiotics. By the 1980s, the window of opportunity for miracle cures had already begun to close. Pharmaceutical companies were under pressure to invent new drugs, while doctors found themselves losing a battle with natural selection. In 2009, an otherwise healthy 20-year-old Brazilian model made international headlines for the last time when she died of a blood infection caused by a common drug-resistant bacterium. In the United States alone, about 100,000 people die from drug-resistant infections every year. The problem of resistance is just one (arguably the worst) of the five major biological threats discussed in this chapter. The others are diarrheal diseases and dengue fever, plus an assortment known as “emerging diseases”—and measles, a disease that few Americans take seriously. Potential complications of these diseases include pneumonia, meningitis, and encephalitis.

MEASLES Summary of Threat Measles is a highly contagious respiratory infection that can lead to life-threatening pneumonia, meningitis, or other complications. Although an effective vaccine is available, and the 2001 Measles Initiative has saved many lives, nearly 200,000 children still die from this disease every year, most of them in the Third World. Crowding, malnutrition, and HIV infection are major risk factors.



Other Names Names for measles include rubeola, morbilli, ten-day measles, nine-day measles, eight-day measles, seven-day measles, red measles, big red measles, and hard measles. The hemorrhagic form is sometimes called black measles. Complications and symptoms associated with measles add more names to the list: Bosin’s disease, Van Bogaert encephalitis, and Dawson’s encephalitis, all rare forms of encephalitis; and Koplik’s spots, lesions that occur inside the mouth before the measles rash appears. The names Edmonston A, Edmonston B, Enders, Schwartz, AIK-C, Connaught, Philips, Beckenham, Moraten, Zagreb, and Belgrade refer to specific strains of the measles virus that researchers have used in developing vaccines. Measles is sarampión in Spanish, griùrach in Scottish Gaelic, spalnièky in Czech, and campak in Indonesian. The Zulu call it isimungumungwane. Some sources confuse measles (rubeola) with other diseases that cause a red rash, such as rubella (German measles) or roseola. Sometimes the word “measles” refers to tapeworm infestation of beef or pork, and the meat thus infested is said to be “measly.”

Description Measles is an airborne respiratory disease that was once a major scourge of childhood. The infectious agent is a virus (Figure 3.1) that infects only humans, but it is closely related to the agents of several animal diseases. In 1941, there were 894,134 reported cases and 2,279 deaths from measles in the United States alone. The true number of cases in 1941 was probably closer to 2 million, as virtually all children contracted measles before the vaccine was invented, and many cases were not reported. Although now infrequent in the United States—there were only 55 reported cases in 2006—measles remains a far more serious disease than many Americans realize.

Figure 3.1 Scanning electron micrograph showing measles (rubeola) virus. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



Table 3.1 Examples of Measles Outbreaks Year


1846 1875 1941–1942 1975 1977–1978 1989–1991 1991 1997 2000 2001–2002 2005 2006

Faeroes Fiji New Haven, CT Greensville, Ontario Shetland, UK United States Israel São Paulo, Brazil Japan Ukraine Chad Catalonia, Spain

Estimated Cases

Estimated Deaths

6,000 135,000 3,200 47 1,032 55,000 1,036 42,055 200,000 25,000 21,812 381

102 36,000 0 0 0 135 0 42 88 14 870 0

Sources: World Health Organization (WHO), U.S. Centers for Disease Control and Prevention (CDC).

Measles is highly infectious, spreading both by airborne droplet inhalation and by direct or indirect contact. Symptoms begin with a slight fever and cough, usually ten to twelve days after exposure. The fever gradually rises, and small whitish spots with red borders may appear inside the mouth. The measles rash starts on the face and spreads downward, eventually covering the body. Other symptoms may include eye irritation, diarrhea, and swollen lymph nodes. After recovery, most people have permanent immunity. About one-third of measles cases involve at least one complication, such as severe diarrhea, ear infections, pneumonia, or seizures. More serious problems, such as meningitis or deafness, occur in about one out of every 1,000 cases. The death rate is usually low, but it varies from one region and outbreak to another (Table 3.1). A rare complication called subacute sclerosing panencephalitis (SSP) can cause death or permanent neurological damage. In a pregnant woman, measles—like several other diseases, including the unrelated German measles—can cause miscarriage and possibly birth defects. Measles can Case Study 3-1: Measles and also activate an existing tuberculosis infection. the Yanomami

Who Is at Risk? Measles is so highly infectious that the only people not at risk during an outbreak are those who have already had measles. Those who were vaccinated at least twice after age 1 are about 90 to 95 percent safe. Complications are least likely to occur in children over age 5 and adolescents. Elderly or malnourished people, babies, and those with weakened immune systems are at highest risk. In underdeveloped nations with high rates of malnutrition and poor healthcare, and in populations with no prior exposure to measles, the case fatality rate may exceed 10 percent (Case Study 3-1).

The 2000 book Darkness in El Dorado claims that American scientists who provided measles vaccination to the South American Yanomami people in 1968 were trying to start an epidemic to test a eugenics theory. It is hard to determine exactly what really happened, except that the Yanomami may have been treated and interviewed without their informed consent, and that many died of measles as a result of contact with outsiders. Some 20 years after this fiasco, a second invasion force visited the Yanomami, this time in the form of gold prospectors who reportedly poisoned the rivers with mercury and introduced malaria, tuberculosis, and other diseases. Regardless of how this story began, it is unlikely to have a happy ending.



The Numbers Before 1963, when the first measles vaccine became available, 500 to 2,000 children died of this disease in a typical year in the United States. Many more children developed encephalitis or other complications that damaged the brain, heart, or eyes. The MMR (measles-mumps-rubella) vaccine greatly reduced the incidence of measles, but not everyone wants this vaccine or has access to it. In 2000, measles caused 757,000 deaths worldwide, most of them in Africa and India. By 2004, however, the global death toll from measles was down to 410,000, and by 2008 it fell to 197,000. The world owes this stunning achievement to worldwide vaccination and health education campaigns sponsored by the 2001 Measles Initiative, a partnership of the American Red Cross, CDC, UNICEF, WHO, and the United Nations. The Initiative’s goal is to reduce measles deaths to 10 percent of the 2000 level by 2010. But even that 10 percent will keep the measles virus alive and able to re-emerge wherever public health vigilance or public cooperation falters.

History Hippocrates (460–375 B.C.) described many diseases, including mumps and scarlet fever, but nothing in his surviving work sounds like measles. Either it had not yet reached Greece, or he did not distinguish it from other common childhood rashes. The Persian physician Razes or Rhazes (Abu Bakr Razi) published a description of measles in the tenth century A.D. He cited earlier sources who believed that measles arrived in the Middle East from Africa during the siege of Mecca in the sixth century A.D., but this claim is hard to evaluate. In 1552, 15-year-old Edward VI of England (son of Henry VIII) caught measles and smallpox in rapid succession, followed by tuberculosis, which ended his life in 1553. American microbiologist Maurice Ralph Hilleman (1919–2005) invented more than 40 vaccines, including the MMR vaccine, the first flu shots, the hepatitis A and B vaccines, the chickenpox vaccine, and many others that are still in use today. When the first attenuated measles vaccine released in 1963 had unacceptable side effects, he developed a safe version that became available in 1965. Dr. Hilleman’s discoveries have saved hundreds of millions of lives, and it is ironic that anti-vaccination crusaders and conspiracy theorists have vilified his work. In 1989–1991, the United States had a measles epidemic, with about 55,000 cases and 135 deaths. Many were children or college students who had never been vaccinated or whose childhood vaccinations were given too early. Although this outbreak represented a small fraction of the annual toll before 1963, opponents of immunization point to the 1989–1991 measles epidemic as proof of the vaccine’s failure. On the contrary, the numbers show that the vaccine is about 95 percent effective. Japan repealed its mandatory vaccination laws in 1994, and many Japanese children have not had a second booster shot. As a result, the country still has large measles epidemics. In 2000, Japan had about 200,000 cases of measles and 88 deaths. In 2008, health officials reported that measles was once again endemic in Britain and showing “continuous spread,” thanks to scare campaigns about autism and MMR vaccine (Case Study 3-2).

Prevention and Treatment Vaccination is recommended for anyone who was born after 1957 and has never had measles. All states require children to be vaccinated twice (after age one and before starting


school), but most states offer religious or personal belief exemptions. Measles vaccines have been available since 1963, but they are not perfect. Both the standard subcutaneous vaccine and a recently developed aerosol vaccine are 90 to 95 percent effective in preventing infection. Unimmunized contacts of measles patients may be vaccinated within 72 hours after exposure. Oral or intravenous ribavirin is sometimes used to treat measles, either alone or in combination with immune globulin. In 2009, animal studies of a new measles DNA vaccine were in progress. If approved, this vaccine might be more effective than those presently in use, particularly in younger children. Since it does not contain live virus, it might also alleviate some safety concerns, whether justified or not.


Case Study 3-2: The 1998 Autism Scare

In 1998, the journal Lancet published what appeared to be evidence of a link between autism and the MMR vaccine. It was every parent’s worst nightmare come true. The authors of the 1998 study later retracted their findings, however, and several other studies have exonerated the vaccine. As of 2009, the consensus is that neither thimerosal (a mercury-containing preservative) nor the MMR vaccine itself causes autism. Yet the controversy has continued, with some parents blaming the vaccine not only for autism but also for epilepsy, arthritis, fatigue, attention deficit disorder, and other conditions.

Popular Culture In the 1995 motion picture Apollo 13, NASA replaced the command module pilot at the last minute because he was exposed to measles. Since he had no history of measles, and thus no immunity, there was concern that he might become ill during the mission. Accounts vary, but apparently the real-life astronaut was exposed to rubella (German measles), not measles. In the 2007 remake of the motion picture I Am Legend, doctors use a genetically engineered measles virus to treat cancer. The virus mutates and escapes, causing a deadly pandemic that somehow turns its victims into the walking dead, who then devote their lives (or deaths or whatever) to the task of infecting the few remaining healthy people on Earth. According to at least one source, the story symbolizes the ongoing struggle between the allegedly indoctrinated zombie-like masses who accept vaccination and the enlightened holdouts who oppose it. In Mark Twain’s 1876 novel Tom Sawyer, Tom contracts measles and is sick for two weeks. A few days after his recovery, Tom has a relapse and is bedridden for another three weeks. The early medical literature reported a few cases of relapsing measles, but modern sources do not recognize this phenomenon. It would appear that Tom developed a secondary infection as a complication of measles. The fact that he felt depressed just before the relapse, and interpreted a thunderstorm as divine retribution for his sins, might suggest encephalitis. In the 1950s and early 1960s, parents often held “measles parties” when one neighborhood child contracted the disease, so all of them could catch it and get it over with. This practice reflected the popular belief that measles was not dangerous; nobody, to the author’s knowledge, ever held diphtheria or polio parties. In the twenty-first century, measles parties reportedly are making a comeback. In North America and northern Europe, folk remedies for measles once included cow dung, roast mouse, mistletoe growing on hawthorn, mare’s milk, bread or tea made from corn shucks, holly leaf tea, chamomile tea, coneflower (Echinacea), the blood of a black hen, or sheep dung mixed with porter ale, sulfur, and water. Traditional Chinese herbal remedies include drinking a concoction of chopped pumpkin vine or Japanese holly fern (Cyrtomium fortunei).



The Future The complete eradication of measles, although possible, remains an elusive dream. The cattle disease rinderpest (Chapter 4) is on the brink of eradication, and it is closely related to measles; but herd immunity is hard to achieve without vaccination, and cows, unlike humans, can be vaccinated without their consent. Although there is little evidence that the measles vaccine causes autism, persistent rumors interfere with public cooperation. Also, since the measles vaccine is less effective in persons with weakened immune systems, the HIV epidemic may complicate the eradication of measles.

References and Recommended Reading Barnard, D. L. “Inhibitors of Measles Virus.” Antiviral Chemistry and Chemotherapy, Vol. 15, 2004, pp. 111–119. Baird, G., et al. “Measles Vaccination and Antibody Response in Autism Spectrum Disorders.” Archives of Disease in Childhood, Vol. 93, 2008, pp. 832–837. Baur, M. P., et al. “International Genetic Epidemiology Society: Commentary on Darkness in El Dorado by Patrick Tierney.” Genetic Epidemiology, Vol. 21, 2001, pp. 81–104. Burgess, D. C., et al. “The MMR Vaccination and Autism Controversy in United Kingdom 1998–2005: Inevitable Community Outrage or a Failure of Risk Communication?” Vaccine, Vol. 24, 2006, pp. 3921–3928. Dabbagh, A., et al. “Progress in Global Measles Control and Mortality Reduction, 2000–2006.” Morbidity and Mortality Weekly Report, Vol. 56, 2007, pp. 1237–1241. Dales, L. G., et al. “Measles Epidemic from Failure to Immunize.” Western Journal of Medicine, Vol. 159, 1993, pp. 455–464. Deer, B. “MMR Doctor Andrew Wakefield Fixed Data on Autism.” The Sunday Times, 8 February 2009. de Quadros, C. A., et al. “Feasibility of Global Measles Eradication After Interruption of Transmission in the Americas.” Expert Review of Vaccines, Vol. 7, 2008, pp. 355–362. Dugger, C. W. “Mothers of Nepal Vanquish a Killer of Children.” New York Times, 30 April 2006. Grais, R. F., et al. “Unacceptably High Mortality Related to Measles Epidemics in Niger, Nigeria, and Chad.” PLoS Medicine, January 2007. Hiremath, G. S., and S. B. Omer. “A Meta-analysis of Studies Comparing the Respiratory Route with the Subcutaneous Route of Measles Vaccine Administration.” Human Vaccines, Vol. 1, 2005, pp. 30–36. “Inquiry Planned into MMR Scare.” United Press International, 23 February 2004. Kumar, V. “Measles Outbreak in Gibraltar, August–October 2008: A Preliminary Report.” Eurosurveillance, 6 November 2008. “Men Against Measles.” Time, 8 August 1960. “New Book, Article Accuses Scientists of Disrupting Yanomami Tribes.” CNN, 2 October 2000. Norrie, J. “Japanese Measles Epidemic Brings Campuses to Standstill.” Sydney Morning Herald, 27 May 2007. Olsson, K. “An Ethics Firestorm in the Amazon.” U.S. News and World Report, 2 October 2000, p. 51. Orenstein, W. A., et al. “Measles Eradication: Is It in Our Future?” American Journal of Public Health, Vol. 90, 2000, pp. 1521–1525. Roosevelt, M. “Yanomami.” Time, 2 October 2000. “Scientists Retract Earlier MMR–Autism Tie.” United Press International, 4 March 2004. Singh, V. K., and R. L. Jensen. “Elevated Levels of Measles Antibodies in Children with Autism.” Pediatric Neurology, Vol. 28, 2003, pp. 292–294. Smith, M. J., et al. “Media Coverage of the Measles-Mumps-Rubella Vaccine and Autism Controversy and Its Relationship to MMR Immunization Rates in the United States.” Pediatrics, Vol. 121, 2008, pp. e836–e843. Station, E., and M. Guran. “The Smoke That Kills.” Links, Vol. 9, 1992, pp. 11–12. Talley, L., and P. Salama. “Short Report: Assessing Field Vaccine Efficacy for Measles in Famine-Affected Rural Ethiopia.” American Journal of Tropical Medicine and Hygiene, Vol. 68, 2003, pp. 545–546. U.S. Centers for Disease Control and Prevention. “Measles—United States, January 1–April 25, 2008.” Morbidity and Mortality Weekly Report, Vol. 57, 2008, pp. 494–498.



Wakefield, A. J., et al. “Ileal-Lymphoid-Nodule Hyperplasia, Non-Specific Colitis, and Pervasive Developmental Disorder in Children.” Lancet, Vol. 351, 1998, pp. 637–641. World Health Organization, et al. “Global Goal to Reduce Measles Deaths in Children Surpassed: Measles Deaths Fall by 60 Per Cent.” Press release, 19 January 2007. “World Measles Deaths Halved in 6 Years.” United Press International, 10 March 2006.

DYSENTERIES AND ENTERIC FEVERS Summary of Threat As a group, waterborne and foodborne diseases that target the human gastrointestinal tract kill more people every year than HIV. Most of these diseases cause diarrhea and dehydration, whereas others can damage the intestine and other organs. Examples include cholera, shigellosis, salmonellosis, typhoid fever, and E. coli. Clean drinking water would prevent most of these deaths. Other Names Diarrhea or dysentery in general is rhyddni (“looseness”) in Welsh, Dünnschiss (“thin feces”) in German, and ishal (“the trots”) in Turkish. Forms of diarrhea that afflict travelers have acquired colorful nicknames, such as the “Rangoon runs,” “Bali belly,” and the “Tijuana two-step.” (These names reflect no discredit on the host nations; visitors to the United States often contract a similar malady here.) English names for the specific diseases in this section include the following. Cholera: Asiatic cholera, Indian cholera, epidemic cholera, blue cholera, spasmodic cholera, cholera asphyxia, or vibriosis. Shigellosis: Bacillary dysentery, bloody flux, Shigella enteritis, Flexner’s dysentery, Japanese dysentery, or Schmidt’s bacillus. Salmonellosis: Salmonella food poisoning, Salmonella enterocolitis, or nontyphoidal salmonellosis. Typhoid and paratyphoid fever together are known as enteric fever or enteromesenteric fever. Specific names for typhoid include typhus abdominalis, cesspool fever, Lent fever, nervous fever, night-soil fever, and Peyerian fever. Specific names for paratyphoid include Schottmüller’s disease and Brion-Kayser disease. Escherichia coli (E. coli): The word “escherichiasis” is hard to pronounce, so most sources refer to the strain instead, such as E. coli O157:H7, diarrheogenic E. coli (DEC), enterohemorrhagic E. coli (EHEC), enteroinvasive E. coli (EIEC), enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), Shiga toxin–producing E. coli (STEC), Shiga toxigenic E. coli (STEC), or verotoxin-producing E. coli (VTEC). Description In the United States, most highly publicized diarrhea outbreaks are traceable to bacteria such as toxigenic E. coli and nontyphoidal Salmonella. In the Third World, shigellosis and cholera cause hundreds of thousands of deaths every year (Table 3.2). Typhoid and paratyphoid fever often damage the intestines, but they do not always cause diarrhea. The fact that Westerners tend to dismiss diarrhea as a social inconvenience should not distract readers from the seriousness of these diseases. Cholera (agent Vibrio cholerae, serogroup O1 or O139): This disease can cause profuse watery diarrhea, severe dehydration, and death within a few hours after onset. Humans appear to be the only animal reservoir, but the bacteria (Figure 3.2) can persist in coastal waters, often in



Table 3.2 Some Outbreaks of Dysentery and Similar Diseases Disease Cholera Cholera Cholera Cholera Cholera E. coli O157 E. coli O157 E. coli O157 Salmonellosis Salmonellosis Salmonellosis Salmonellosis Shigellosis Shigellosis Shigellosis Typhoid Typhoid Typhoid Typhoid

Year 1849 1849 1854 1991–1999 2008–2009 1994 1999 2002 1965 2007–2008 2008 2008–2009 1997 1998 2005 1964 1996–1998 2004 2005

Location Chicago, IL Canada Chicago, IL South America Zimbabwe Washington Albany, NY Pennsylvania Riverside, CA United States Estonia United States Lubbock, TX Minnesota Spain Scotland Tajikistan D.R. Congo South Africa

Estimated Cases

Estimated Deaths

NR NR NR 1 million 100,000+ 501 1000+ 51 15,000 1,442 94 600+ 480 83 196 500+ 24,000 42,564 400+

Sources: World Health Organization (WHO), U.S. Centers for Disease Control and Prevention (CDC).

Figure 3.2 Micrograph showing a Vibrio cholera strain that causes cholera. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

678 6,000 1,424 10,000 4,300+ 3 2 0 3 2 0 11+ 0 0 0 0 NR 214 3



association with small crustaceans called copepods. Cholera is usually curable with prompt Case Study 3-3: A Death in Florence treatment, but in Third World countries where Leland Stanford Jr. died of typhoid fever in cholera is prevalent, clean rehydration fluids are Florence, Italy, on 13 March 1884, two often unavailable. months before his sixteenth birthday, while Shigellosis (agents Shigella dysenteriae, S. he and his parents were on a Grand Tour of flexneri, S. boydii, and S. sonnei): This disease Europe. He caught the disease in Constantinople, where they had gone because the causes bloody diarrhea (dysentery) with a fever sultan wanted Leland Sr.’s advice about and abdominal cramps. Typical sources are conbuilding a railroad. The family returned to taminated water or vegetables fertilized with raw Florence for treatment, but all efforts failed. sewage. The bacteria produce the Shiga toxin, The night after his death, the young man which causes these symptoms by inhibiting proappeared to his father in a dream and said: tein synthesis. This toxin (but not the Shigella “Do not say that you have nothing to live bacterium itself) is classified as a biosecurity for . . . Father, serve humanity.” Mr. Stanford threat under the Bioterrorism Protection Act of woke from his dream and told his wife, 2002. Reactive arthritis may develop months “The children of California shall be our chilor years after recovery from shigellosis. dren.” The couple founded Stanford UniverSalmonellosis (agent Salmonella enterica, sity to honor their son’s memory. several serovars): This disease is usually foodborne, but there are other ways to catch it—for example, by touching a live turtle or a raw chicken, and then putting the same hand in your mouth. The disease causes profuse watery diarrhea, sometimes with vomiting, headache, and/or abdominal pain. Reactive arthritis may develop months or years later. The case fatality rate, however, is less than 1 percent. Typhoid (agent Salmonella typhi): Symptoms of this waterborne and foodborne disease include high fever, headache, a rash of flat pink spots, and an enlarged spleen. Either diarrhea or constipation may occur, and the intestine may bleed or become perforated. About 10 to 20 percent of untreated patients die (Case Study 3-3). Paratyphoid (agent Salmonella paratyphi) is similar but less severe. Both diseases affect only humans, who can become lifelong carriers, like the famous Typhoid Mary. E. coli (agent, Escherichia coli O157:H7 and others): Most strains of this bacterium (Figure 3.3) are normal, harmless occupants of the mammalian intestine, but some produce a dangerous toxin. People have contracted this disease from unpasteurized milk or juice, contaminated ground beef, lake water, airborne sawdust in a dirty building, and therapy dogs fed on raw meat. Severe cases can cause kidney failure and death. Most cases are relatively mild, but survivors may develop kidney damage or pancreatitis years after infection.

Who Is at Risk? Children, malnourished persons, those with low incomes or limited education, those who live under crowded conditions, and those with compromised immune systems are all at increased risk from diarrheal diseases in general. The following paragraphs describe additional risk factors for specific diseases. Persons with blood group O, and those with below-average levels of stomach acid, are at increased risk for cholera. Disasters contribute to cholera outbreaks by contaminating water sources and disrupting sanitation services. Breastfed infants have some protection, either because of maternal antibodies or because they do not drink contaminated water. Survivors have some resistance to reinfection with the same strain.



Figure 3.3 Scanning electron micrograph showing Escherichia coli bacteria of the strain O157:H7, which produces a toxin that can cause severe bloody diarrhea in humans. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

A 2007 study of shigellosis in Vietnam showed that households located near a river or a hospital, and those that practiced ancestor worship, were at highest risk. The first two factors may be attributable to water pollution or improper waste disposal; the third is unclear, but may reflect socioeconomic status. Nontyphoidal salmonellosis is hard to avoid, because almost any food, drink, or pet might be a source. In 1996, some 224,000 people in the United States contracted salmonellosis from one contaminated batch of ice cream, while 50 others caught it by touching a fence surrounding a zoo exhibit of Komodo dragons. Persons with below-average levels of stomach acid are at increased risk for typhoid fever. In endemic areas, children and adolescents are most likely to develop severe illness. Persons with cystic fibrosis may be less susceptible to typhoid. Elderly people appear to be at highest risk of contracting E. coli, possibly as a result of low stomach acid secretion. Children are at highest risk for a complication called hemolytic uremic syndrome (HUS), in which red blood cells rupture and capillaries become blocked, often resulting in kidney failure.

The Numbers In 2004, WHO reported 101,383 cases of cholera worldwide, with 2,345 deaths. In 2009, one outbreak in Zimbabwe alone caused 4,127 deaths. The incidence varies from year to year, and many cases go unreported.



There are about 25,000 reported cases of Case Study 3-4: Egg Wars shigellosis each year in the United States, but the actual total is probably much higher. Worldwide, In 1988, British author and former Member there are an estimated 165 million cases each of Parliament Edwina Currie was forced to year, with about 1 million related deaths. resign her position as Junior Health MinisThere are about 50,000 to 100,000 reported ter after angering the poultry industry with a statement that “most of the egg produccases of salmonellosis in the United States in a tion in this county, sadly, is now affected typical year. There are an estimated 38 unrewith salmonella.” Whether or not the stateported mild cases for every one reported. About ment was defensible at the time, it caused 6 percent of cases result from handling amphibegg sales to plummet, forcing the governians or reptiles. Many others result from eating ment to pay millions of pounds in compenraw eggs (Case Study 3-4). sation to poultry farmers. But a 1989 report Typhoid causes about 13 to 21 million cases concluded that Currie was right. The worldwide each year, with 300,000 to 500,000 British government had, in fact, covered up deaths. The United States has only 400 to 500 a recent salmonellosis epidemic, during typhoid cases in a typical year. which salmonella could be recovered from The infamous O157:H7 strain of E. coli any cooked egg with liquid yolk. caused about 73,000 illnesses and 60 deaths in the United States in 2002. For example, in 1999, at the Washington County Fair, near Albany, New York, more than 1,000 people became ill and two died from E. coli infections after drinking contaminated well water.

History The first recorded cholera pandemic was in Asia in 1816. Others followed in 1829, 1852, 1863, 1881, and 1899. The seventh pandemic began in Indonesia in 1961, and a closely related strain that turned up in South America in 1991 is sometimes called the eighth pandemic. The disease might have reached South America in ballast water from a ship, but the reasons for its rapid spread and high mortality have become controversial (see Chapter 7, page 254). In 2008–2009, the collapse of Zimbabwe’s healthcare system and infrastructure resulted in a cholera outbreak that grew rapidly into a major epidemic. Several thousand people died (Table 3.2), although cholera is normally curable with simple rehydration. During World War II, before antibiotics were available, German bacteriologists found that infusions of Bacillus subtilis fed to troops in northern Africa helped control shigellosis. The so-called hay bacillus has remained a popular component of alternative medicine and biological control. Contrary to rumor, the bacterial genus Salmonella was not named for a spoiled fish loaf in the back of someone’s refrigerator. The name is a patronymic to honor American veterinary pathologist Daniel Elmer Salmon (1850–1914), the administrator of a USDA program that discovered a form of salmonellosis in swine. In 2009, the U.S. Food and Drug Administration (FDA) traced a Salmonella outbreak to a peanut butter processing plant in Georgia. Inspectors reported that the firm knowingly shipped contaminated peanut products. There were large leaks in the roof directly above open product containers; the same sink reportedly was used to wash hands, utensils, and mops; and a storage area was coated with “a slimy, black-brown residue.” No discussion of typhoid would be complete without the story of Typhoid Mary, aka Mary Mallon (1869–1938), a New York cook who insisted that germs did not cause disease. If Mary were alive today, she would probably have a website to showcase her beliefs and protest her treatment at the hands of the public health establishment. But an autopsy revealed that Mary’s gallbladder



contained a thriving colony of typhoid bacteria, and during her career as a cook, she infected at least 47 people and caused three deaths. She refused to change occupations and died in quarantine. The first known E. coli O157:H7 outbreaks were in 1982. Some scientists believe the strain originated in Central America in the 1970s, when a bacterial virus transferred a toxin-producing gene from Shigella to the intestinal bacteria of cattle. Others have implicated the cholera bacterium as the source of the gene. Whatever its origin, O157:H7 does not harm infected cattle, but in humans it is sometimes lethal.

Prevention and Treatment Severe diarrhea sometimes clears the gut of normal bacteria that aid in digestion, produce certain vitamins, and provide other useful services. Researchers have proposed that the role of the human appendix may be to store a backup supply of these bacteria. Since most diarrheal diseases are waterborne or foodborne, the best preventive measures include water treatment and sanitary food preparation. In 2008, the FDA allowed irradiation of vegetables to kill bacteria. A zinc supplement may also help prevent and treat diarrhea in children. A study in Bangladesh showed that filtering water through old sari cloth reduced the number of cholera cases by about half. The existing live attenuated single-dose cholera vaccine is only about 70 percent effective, but cholera is fairly simple to treat where rehydration fluids and other basic medical supplies are available. Antimicrobial drugs such as tetracycline or trimethoprim-sulfamethoxazole may shorten the course of the disease. As of 2009, no shigellosis vaccine was licensed for use outside China, but candidate vaccines were in clinical trials. Treatment consists of rehydration, electrolyte replacement, and oral antibiotics such as ciprofloxacin in adults or trimethoprim-sulfamethoxazole in children. Salmonellosis usually requires no treatment other than rehydration and electrolyte replacement. The bathroom will also need cleaning, in this or any other acute diarrheal disease; studies have shown that Salmonella can survive for weeks in biofilms inside toilet bowls. Antibiotic therapy is not recommended except for high-risk groups. In a 2002 study of a salmonella outbreak, 100 percent of exposed people who drank only nonalcoholic beverages became sick, but a mere 78 percent of those who had one or two alcoholic drinks became sick. Alcohol (particularly white wine) stimulates gastric secretion of acid, thus creating a lethal environment for bacteria. Another possibility is that some of the people were simply too drunk to realize they were sick. Typhoid vaccination (available since about 1899) is recommended for those at high risk of exposure to typhoid fever. Most cases are treatable with antimicrobial drugs such as ciprofloxacin, chloramphenicol, ampicillin, or trimethoprim-sulfamethoxazole. In 2009, doctors in Michigan were testing a vaccine to protect against enterotoxigenic E. coli. The usual treatment is rehydration and electrolyte replacement, but severe cases or complications may require hospital treatment. It is unclear whether antimicrobial drugs such as fluoroquinolones are helpful or not. Another new approach is vaccination of cattle to prevent shedding of E. coli O157:H7.

Popular Culture An ever-popular urban legend claims that an unknown evildoer is mailing sponges contaminated with “the Klingerman virus” to random victims, who then contract severe or fatal dysentery.



There is no such virus, but anyone who receives an unexpected sponge should probably discard it anyway. Cocoa has been a popular diarrhea remedy in South America and Europe for centuries. It might actually work, since cocoa contains flavonoids that can inhibit diarrhea. Other sources recommend eating fenugreek seeds, cheese, or nuts. People who feel well enough to eat these foods will probably recover with or without them. Chinese herbal remedies for shigellosis include concoctions of siler (Siler divaricatum), purple giant hyssop (Agastache rugosa), snow rose (Serissa foetida), Chinese buttonbush (Adina rubella), or huang-qi (Astragalus henryi). For typhoid, Chinese herbalists recommended black cardamom (Amomum costatum), sweet flag (Acorus sp.), bai zhu (Atractylis ovata), and other herbs, with the addition of rhinoceros or buffalo horn in the event of intestinal bleeding. In nineteenth-century Europe and North America, one standard treatment for enteric fever (typhoid) was to cover the patient with a poultice of horse dung. Another was to tie fish to the patient’s feet, or tie cabbage leaves around his neck, or wrap him in a fresh, warm sheepskin, immediately after removing it from the sheep. It’s amazing that anyone survived medical treatment in those days. In the 1985 novel and 2007 motion picture Love in the Time of Cholera, the main character’s husband is a doctor who treats cholera. In the 1997 movie Contagious, an epidemiologist investigates a cholera epidemic and traces it to airline food. One of the most startling T-shirts ever designed features a covered wagon and the words: “You have died of dysentery.” This slogan refers to a classic computer game called Oregon Trail, in which players try to reach their simulated destination without succumbing to the diseases that ended the lives of many settlers. Since E. coli first made headlines in 1982, the disease has had little opportunity to find its way into popular culture. In the 1998 motion picture Urban Legend, one character says to another: “If we ever have another E. coli crisis in the cafeteria, I want you to have the biggest, juiciest burger. My treat.” The following urban legend appeared on the Web in 2007: “It has been scientifically proven that if we drink 1 liter of water each day, at the end of the year we would have absorbed more than 1 kilogram of Escherichia coli.” In fact, to achieve this level of consumption it would be necessary to drink untreated sewage. (This claim refers to coliform bacteria in general, not the toxigenic strains that cause dysentery.) The Future In 2009, about 1 billion people lacked access to safe drinking water, and about 80 percent of all illnesses in the Third World were related to this problem. While the literature on this subject grows, the water supply shrinks. Water is a renewable resource, but that fact does not make it potable. The reasons for this problem include overpopulation, crumbling infrastructure, political instability, industrial waste, climate change, and local custom. More than 3 million people die every year from the effects of diarrhea and related diseases, and the cost of treating survivors and supporting their economies may exceed the cost of preventive measures, such as water filters and health education.

References and Recommended Reading “Anti-Typhoid Vaccine.” New York Times, 9 February 1913. Barker, J., and S.F. Bloomfield. “Survival of Salmonella in Bathrooms and Toilets in Domestic Homes Following Salmonellosis.” Journal of Applied Microbiology, Vol. 89, 2000, pp. 137–144. Bercu, T. E., et al. “Amebic Colitis: New Insights into Pathogenesis and Treatment.” Current Gastroenterology Reports, Vol. 9, 2007, pp. 429–433.



Bhattacharya, S. K. “Progress in the Prevention and Control of Diarrhoeal Diseases since Independence.” National Medical Journal of India, Vol. 2003, pp. 15–19. Bruce, M. G., et al. “Lake-Associated Outbreak of Escherichia coli O157:H7 in Clark County, Washington, August 1999.” Archives of Pediatrics and Adolescent Medicine, Vol. 157, 2003, pp. 1016–1021. Chen, X., et al. “Differences in Perception of Dysentery and Enteric Fever and Willingness to Receive Vaccines among Rural Residents in China.” Vaccine, Vol. 24, 2006, pp. 561–571. “Dark Chocolate Helps Diarrhea.” Press Release, Children’s Hospital and Research Center at Oakland, California, 29 September 2005. “Evolution of Typhoid Bacteria Traced.” United Press International, 28 November 2006. “FDA: OK to Zap Spinach, Lettuce with Radiation.” Associated Press, 21 August 2008. Forsberg, B. C., et al. “Diarrhoea Case Management in Low- and Middle-Income Countries—An Unfinished Agenda.” Bulletin of the World Health Organization, Vol. 85, 2007, pp. 42–49. Gaffga, N. H., et al. “Cholera: a New Homeland in Africa?” American Journal of Tropical Medicine and Hygiene, Vol. 77, 2007, pp. 705–713. Green, L. R., et al. “Beliefs about Meals Eaten Outside the Home as Sources of Gastrointestinal Illness.” Journal of Food Protection, Vol. 68, 2005, pp. 2184–2189. Griffith, D. C., et al. “Review of Reported Cholera Outbreaks Worldwide, 1995–2005.” American Journal of Tropical Medicine, Vol. 75, 2006, pp. 973–977. Holt, K. E., et al. “High-Throughput Sequencing Provides Insights into Genome Variation and Evolution in Salmonella typhi.” Nature Genetics, Vol. 40, 2008, pp. 987–993. Kato, Y., et al. “Multidrug-Resistant Typhoid Fever Outbreak in Travelers Returning from Bangladesh.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1954–1955. Kim, D. R., et al. “Geographic Analysis of Shigellosis in Vietnam.” Health & Place, Vol. 14, 2008, pp. 755–767. King, A. A., et al. “Inapparent Infections and Cholera Dynamics.” Nature, Vol. 454, 2008, pp. 877–880. Kweon, M. N. “Shigellosis: The Current Status of Vaccine Development.” Current Opinion in Infectious Diseases, Vol. 21, 2008, pp. 313–318. Lockary, V. M., et al. “Shiga Toxin-Producing Escherichia coli, Idaho.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1262–1264. Lucas, R. “Clinical Significance of the Redefinition of the Agent of Amoebiasis.” Revista Latinoamericana de Microbiología, Vol. 43, 2001, pp. 183–187. Millward, D. “Currie ‘Was Right’ on Salmonella.” Telegraph, 26 December 2001. Muniesa, M., et al. “Occurrence of Escherichia coli O157:H7 and Other Enterohemorrhagic Escherichia coli in the Environment.” Environmental Science and Technology, Vol. 40, 2006, pp. 7141–7149. Neergard, L. 2008. “Food Poisoning’s Legacy.” Associated Press, 22 Jan 2008. Nicolas, X., et al. “Shigellosis or Bacillary Dysentery.” Presse Médicale, Vol. 36, 2007, pp. 1606–1618. [French] Nullis, C. “Zimbabwe’s New Export: Cholera.” Associated Press, 26 November 2008. Ochiai, R. L., et al. “A Study of Typhoid Fever in Five Asian Countries: Disease Burden and Implications for Controls.” Bulletin of the World Health Organization, Vol. 86, 2008, pp. 260–268. Petri, W., et al. “Enteric Infections, Diarrhea, and Their Impact on Function and Development.” Journal of Clinical Investigation, Vol. 118, 2008, pp. 1277–1290. “Purpose of Appendix Believed Found.” Associated Press, 5 October 2007. Sanders, J. W., et al. “Military Importance of Diarrhea: Lessons from the Middle East.” Current Opinion in Gastroenterology, Vol. 21, 2005, pp. 9–14. Santamaria, J., and G. A. Toranzos. “Enteric Pathogens and Soil: A Short Review.” International Microbiology, Vol. 6, 2003, pp. 5–9. Schneider, J., et al. “Escherichia coli O157:H7 Infections in Children Associated with Raw Milk and Raw Colostrums from Cows—California, 2006.” Morbidity and Mortality Weekly Report, Vol. 57, 2008, pp. 625–628. Shukla, V. K., et al. “Carcinoma of the Gallbladder—Is It a Sequel of Typhoid?” Digestive Diseases and Sciences, Vol. 45, 2000, pp. 900–903. Snow, M., et al. “Differences in Complement-Mediated Killing of Entamoeba histolytica Between Men and Women—an Explanation for the Increased Susceptibility of Men to Invasive Amebiasis?” American Journal of Tropical Medicine and Hygiene, Vol. 78, 2008, pp. 922–923.



Sur D., et al. “Shigellosis: Challenges and Management Issues.” Indian Journal of Medical Research, Vol. 120, 2004, pp. 454–462. Taylor, R. H. “Cholera and the Royal Navy 1817–1867.” Journal of the Royal Naval Medical Service, Vol. 83, 1997, pp. 147–156. U.S. Centers for Disease Control and Prevention. 2008. Investigation of Outbreak of Infections Caused by Salmonella saintpaul. Updated 18 June 2008. “Vaccine for E. coli Developed.” United Press International, 16 April 2009. Varma, J. K., et al. “An Outbreak of Escherichia coli O157 Infection Following Exposure to a Contaminated Building.” Journal of the American Medical Association, Vol. 290, 2003, pp. 2709–2712. “WHO Calls for Aid for Cholera Outbreak.” United Press International, 6 February 2009. World Health Organization. “Prevention and Control of Cholera Outbreaks: WHO Policy and Recommendations.” 25 November 2008.

DENGUE AND DENGUE HEMORRHAGIC FEVER Summary of Threat Dengue is a mosquito-borne viral disease that causes pain and fever. About 100 million people contract dengue every year, but until recently the death rate was very low. A more dangerous form called dengue hemorrhagic fever (DHF) is becoming more common, possibly as a result of climatic or demographic changes that favor repeated exposures to multiple strains. As of 2009, no vaccine or specific treatment is available. Other Names The correct pronunciation is “DENG-gay,” not “DENG-yoo” or “DENG-goo.” Some people omit the second syllable and pronounce it “deng,” by analogy to words such as “tongue” and “meringue.” Other names include breakbone fever, bone-break fever, stiffneck fever, bonecrushers’ disease, dandy fever, three-day fever, five-day fever, seven-day fever, duengero, broken wing, African fever, and saddleback fever. (“Saddleback” refers to the fact that a graph of the fever sometimes reaches two peaks separated by a dip.) The first four names may also refer to influenza, malaria, or any disease that causes chills, fever, and pain. Less common names for dengue are denguis, tootia, Aden fever, bouquet fever, date fever, polka fever, solar fever, scarlatina rheumatica, febris exanthematica articularis, and exanthesis arthrosia. A 1901 medical text lists nearly 100 names for dengue. Severe forms are known as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Some English dictionaries claim that we owe the name of this disease to the Swahili phrase ka dinga pepo, meaning “cramps brought on by an evil spirit.” (According to a Swahili dictionary, dinga means a car, but dege means cramps.) Other sources claim that dengue is an Indian, Spanish, or Arabic word. Names for dengue in other languages include trópusi náthaláz (“tropical fever”) in Hungarian, calentura roja (“red fever”) in Spanish, Fuenftage-Fieber (“five-day fever”) in German, and fièvre épidémique inflammatoire (“epidemic inflammatory fever”) in French. Description We debated whether dengue belongs in a book on biological threats, because until recently the death rate was very low—except in rare cases when it progressed to dengue hemorrhagic



fever (DHF), which can kill 10 to 20 percent of untreated patients. A few years ago, however, doctors made the unsettling discovery that DHF is no longer rare. In Mexico, its reported incidence increased by 600 percent between 2001 and 2007. Also, dengue is one of several diseases that may expand its range as a result of global climate change (Chapter 6). Dengue symptoms include sudden onset of fever with severe joint and muscle pain. Vomiting and diarrhea may occur, and a rash of small red spots often appears on the legs and chest. The dengue virus (a flavivirus similar to the agent of hepatitis C) has four distinct serological types: DENV-1, DENV-2, DENV-3, and DENV-4. A person who survives infection with one type of dengue becomes immune to that type only; if he or she later contracts another type, the immune system sometimes overreacts, causing DHF. Urbanization and travel have helped expand the range of dengue and have increased the probability of contracting more than one type. The international trade in used tires may also spread the disease, since tires trap water in which mosquito vectors can breed. DHF symptoms include bleeding or bruising that results from an increase in vascular permeability. Complications such as dengue encephalitis and dengue hepatitis may also occur. DHF is classified according to the following grades: • • • •

Grade I: Fever and minor hemorrhagic symptoms (positive tourniquet test or easy bruising). Grade II: Grade I symptoms plus spontaneous bleeding from skin or mucous membranes. Grade III: General circulatory failure; rapid, weak pulse, low blood pressure. Grade IV: Profound shock, undetectable blood pressure or pulse.

Dengue does not spread directly from one person to another. The vectors are mosquitoes in the genus Aedes, usually Aedes aegypti or A. albopictus (Figure 3.4). These insects are active in the daytime, often prefer urban areas, and have the peculiar habit of biting people on the ankles. To transmit dengue, a mosquito must survive for 10 to 14 days after taking blood from an infected person. Meanwhile, the mosquito continues to take blood meals while the virus multiplies inside its body. Once the virus reaches high enough levels, it finds its way into the bloodstream of the mosquito’s next target. A 2008 study showed that wild rodents, bats, and marsupials near cities may serve as a reservoir. Nonhuman primates may also be hosts in some areas.

Who Is at Risk? Worldwide, about 2.5 billion people are at risk for dengue. In the United States, recent autochthonous transmission—that is, transmission in the same place where the outbreak occurs—has been documented only in Texas and Hawaii. Many cases probably go unreported, since mild dengue resembles flu. Aedes mosquitoes capable of transmitting dengue are abundant year-round in many American cities, such as Tucson, Arizona, but not enough local residents are infected to start an outbreak. As noted above, people who have already had dengue are at increased risk of DHF if they are exposed to a second dengue serotype. In 1977, for example, Cuba had an epidemic of DEN1. When a DEN-2 epidemic visited the island in 1981, people who were immune to DEN-1 from the previous epidemic were nearly four times more likely to contract DHF than people who had no immunity at all. A study of dengue risk factors in Laredo, Texas, and neighboring Nuevo Laredo, Mexico, showed that the higher risk in Mexico was largely attributable to the use of evaporative coolers



Figure 3.4 The mosquito Aedes mediovittatus is a known vector of dengue fever in humans. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

instead of air conditioners. The dry, cool environment inside air-conditioned buildings is hostile to Aedes mosquitoes. The investigators found that 55 percent of dengue cases in Nuevo Laredo would not have occurred if all households had air conditioning. However, medical records showed that at least ten Laredo residents sought treatment for dengue (as later confirmed by blood tests), but received a diagnosis of “flu-like illness.” In other words, part of the reason for the absence of dengue north of the border is that doctors are simply not familiar with the disease (Case Study 3-5).

The Numbers Dengue infects 50 to 100 million people every year, but about 90 percent develop no symptoms or report mild flu-like symptoms. On average, about 500,000 people are hospitalized with



Case Study 3-5: NAFTA and Dengue Among the many criticisms leveled at the North American Free Trade Agreement (NAFTA) of 1992 is the claim that immigrants and visitors will bring tropical diseases with scary names into the United States. Dengue, malaria, typhoid, cholera, yellow fever, and leprosy are the diseases most often cited as examples in antiNAFTA literature, but dengue is the only one of these that appears to pose a significant threat north of the border. Studies suggest that even dengue is more amenable to vector control programs, home air conditioners, and window screens than to border security.

dengue every year. Although the death rate is low (some 20,000 worldwide in a typical year), dengue is numerically the most important vectorborne viral disease of humans (Table 3.3). The case fatality rate in each outbreak depends on the serotypes involved, the availability of treatment, and the accuracy of reporting. In dengue shock syndrome (DSS), mortality can be as high as 40 percent. Cuba reported 354,515 dengue cases in 1981, with an estimated 24,000 cases of DHF, 10,000 cases of DSS, and 158 deaths. In 2000, Brazil reported 288,245 dengue cases with 91 deaths.


A Chinese medical encyclopedia published in A.D. 992 described a disease similar to dengue. Outbreaks reportedly took place in the French West Indies in 1635 and in Panama in 1699. In 1771, a Spanish doctor in Puerto Rico wrote about a fever called quebranta huesos (“it breaks bones”), probably a reference to dengue. Yet dengue was not well known until 1779, when major outbreaks occurred in northern Africa, Spain, and India. In 1780, the disease spread to North America on a ship, and Philadelphia had a large epidemic. By 1801, when Queen Luisa of Spain caught dengue and described it in a series of letters, the name and the disease apparently were widely recognized. After World War II, a dengue pandemic began in southeast Asia and spread around the globe. Doctors became aware of dengue hemorrhagic fever (DHF) in the 1950s during dengue epidemics in the Philippines and Thailand. Vector control programs eliminated Aedes aegypti from many countries in the 1960s, but its range expanded again after these programs ended. The first known major DHF epidemic occurred in Cuba in 1981. Table 3.3 Some Outbreaks of Dengue and Dengue Hemorrhagic Fever Year


1981 1989–1990 1994 1996 1998 1998 2000 2001–2002 2002 2002 2006 2007 2008 2009

Cuba Venezuela Nicaragua Delhi, India Argentina Vietnam Bangladesh Hawaii Malaysia Easter Island, Chile India Jamaica Rio de Janeiro, Brazil Bolivia

Estimated Cases

Estimated Deaths

354,515 6,000+ 20,469 8,900 818 119,429 5,575+ 122 32,289 636 12,317 4,260 55,000 56,000+

Sources: World Health Organization (WHO), U.S. Centers for Disease Control and Prevention (CDC).

158 78 6 374 0 342 90 0 74+ 0 184 18 67 25+



Prevention and Treatment Dengue is a complicated disease to prevent or treat. Aedes mosquitoes are hard to avoid because they are active in the daytime, but people in endemic areas can use insect repellents and protective clothing. Mosquito control might sound like a no-brainer; however, a 2008 study showed that partially eliminating vectors might actually increase the incidence of DHF. Adult Aedes mosquitoes often live inside houses, but air conditioners (not evaporative coolers) greatly reduce risk. It is also important to eliminate containers of water where mosquitoes can breed. Mosquito fish (Gambusia and others) and small crustaceans called copepods can remove mosquito larvae from ponds, but even underground septic tanks can serve as habitat. In 2009, researchers reported preliminary success in controlling Aedes mosquitoes by infecting them with a bacterial symbiont that shortens the adult lifespan. Efforts to develop a vaccine have been unsuccessful, mainly because of the existence of four different serotypes. One possible solution, proposed by Rice University researchers in 2008, would be to develop four vaccines and inject them simultaneously at different locations on the body. As of 2009, at least two major pharmaceutical companies and several government agencies (including the U.S. Army) were working to develop dengue vaccines. Once a person contracts dengue, treatment is mainly supportive. Corticosteroids apparently are not helpful in preventing shock. Patients should not take aspirin or other anticoagulant drugs without consulting a physician because of the danger of increased bleeding.

Popular Culture The Consul’s File, a 1977 novel by Paul Theroux, describes the feverish visions of a young American teacher who contracts dengue in Malaysia and nearly dies. The same author also explored this theme in his 1975 short story “Dengue Fever,” a dark tale of fever and the supernatural. Another Theroux novel, The Mosquito Coast, inspired the 1986 motion picture with Harrison Ford as an obsessive inventor-turned-survivalist. After inventing a machine that uses fire to create ice, he moves his family to coastal Honduras, a region with a high incidence of dengue and malaria. He expects his gift of ice to transform this pristine tropical wilderness into paradise, by cooling homes and promoting health, but things don’t work out that way. Instead, one necessity follows another, air conditioning and mosquito nets and patriarchy and violence, until at last he finds himself on the verge of recreating the very world he has rejected. One traditional cure for dengue fever is raw pegaga leaf juice. Pegaga or ulam pegaga (Centella asiatica) grows wild in many parts of Asia and is a popular cure for many ailments, particularly those that tend to resolve in a few days without treatment. Other sources claim that the miracle dengue cure is papaya leaf juice (or tea). A plant called boneset (Eupatorium perfoliatum) was once popular in the southern United States as a treatment for the pain and fever of dengue and other illnesses. People kept bouquets of dried boneset hanging from the house rafters to remind children to dress warmly and keep dry, in order to avoid getting sick and being required to drink bad-tasting boneset tea. For a poetic advertisement involving dengue, see Case Study 3-6.

The Future Some authorities predict that dengue will expand its range into the United States as a result of global warming, immigration, and international travel. Others point out that dengue was here



Case Study 3-6: Dengue Doggerel The following poem, which appeared in the Vicksburg (Mississippi) Herald newspaper in 1873, illustrates public perceptions of dengue in the American South of that era, before the advent of dengue hemorrhagic fever and NAFTA. The poet was not named, but we can probably rule out Sidney Lanier: Silent and cold on his lonely cot the lover bold did lay, His limbs were stiff, and the dengue pains had wasted his form away. While the fever raged he cried aloud, in incoherent strain “Oh, that my drooping eyes might see that angel face again!” He cried in the anguish of dengue pain for a sight of his love once more, Till her heart was touched and she came to the side of his bed, which was spread on the floor. Through dreary days and weary nights she sat by her lover’s couch, And proved that at nursing and tending him she wasn’t any slouch. She soothed his spirit and drove away all trace of dengue blues, By reading the Herald every day aloud— all the local news.1

before, and that our air conditioners chased it away. What the world really needs is an effective tetravalent vaccine that would make it possible to eradicate the disease. Also, since doctors outside endemic areas often fail to recognize dengue, a better diagnostic test is needed. Otherwise, undiagnosed dengue might be transferred through blood transfusions.

References and Recommended Reading

Barrera, R., et al. “Unusual Productivity of Aedes aegypti in Septic Tanks and Its Implications for Dengue Control.” Medical and Veterinary Entomology, Vol. 22, 2008, pp. 62–69. Barreto, M. L., and M. G. Teixeira. “Dengue Fever: A Call for Local, National, and International Action.” Lancet, Vol. 372, 2008, p. 205. daSilva, L., and R. Richtmann. “Vaccines under Development: Group B Streptococcus, HerpesZoster, HIV, Malaria and Dengue.” Jornal de Pediatria, Vol. 82, 2006, pp. S115–124. de la Sierra, B., et al. “Race: A Risk Factor for Dengue Hemorrhagic Fever.” Archives of Virology, Vol. 152, 2007, pp. 533–542. Domingo-Carrasco, C., and J. Gascon-Bustrenga. “Dengue and Other Hemorrhagic Viral Fevers.” Enfermedades Infecciosas y Microbiologia Clinica, Vol. 23, 2005, pp. 615–626. Fuller, T. “The War on Dengue Fever.” New York Times, 3 November 2008. Gibbons, R. V., and D. W. Vaughn. “Dengue: An 1 Northern Vindicator, 6 December 1873. Escalating Problem.” British Medical Journal, Vol. 324, 2002, pp. 1563–1566. Gould, E. A., and T. Solomon. “Pathogenic Flaviviruses.” Lancet, Vol. 371, 2008, pp. 500–509. Gubler, D. J. “Dengue/Dengue Hemorrhagic Fever: History and Current Status.” Novartis Foundation Symposium, Vol. 277, 2006, pp. 3–16. Gulati, S., and A. Maheshwari. “Atypical Manifestations of Dengue.” Tropical Medicine and International Health, Vol. 12, 2007, pp. 1087–1095. Halstead, S. B. “Dengue.” Lancet, Vol. 370, 2007, pp. 1644–1652. Janes, C. R. “Theorizing Global-Local Linkages in Global Health Studies.” Paper presented to the 2003 Fulbright Visiting Scholars Conference, “International Cooperation in a Borderless World,” Washington, DC, 2–5 April 2003. Katz, T. M., et al. “Insect Repellents: Historical Perspectives and New Developments.” Journal of the American Academy of Dermatology, Vol. 58, 2008, pp. 8865–8871. Leong, A. S., et al. “The Pathology of Dengue Hemorrhagic Fever.” Seminars in Diagnostic Pathology, Vol. 24, 2007, pp. 227–236. Lo, R. V., and S. J. Gluckman. “Fever in the Returned Traveler.” American Family Physician, Vol. 68, 2003, pp. 1343–1350. Lum, L. C. “Dengue Encephalitis: A True Entity?” American Journal of Tropical Medicine and Hygiene, Vol. 54, 1996, pp. 256–259.



Maroun, S. L., et al. “Case Report: Vertical Dengue Transmission.” Jornal de Pediatria, 23 October 2008. McMeniman, C. J., et al. “Stable Introduction of a Life-Shortening Wolbachia Infection into the Mosquito Aedes aegypti.” Science, Vol. 323, 2009, pp. 141–144. Nobuchi, H. “The Symptoms of a Dengue-like Illness Recorded in a Chinese Medical Encyclopedia.” Kanpo Rinsho, Vol. 26, 1979, pp. 422–425. [Japanese.] Noqueira, R. M., et al. “Dengue Viruses in Brazil, 1986–2006.” Pan American Journal of Public Health, Vol. 22, 2007, pp. 358–363. Ooi, E. E., et al. “Dengue Prevention and 35 Years of Vector Control in Singapore.” Emerging Infectious Diseases, Vol. 12, 2006, pp. 887–893. Peña, G., et al. “Underdiagnosis of Dengue—Laredo, Texas, 1999.” Lancet, Vol. 285, 2001, p. 877. Rigau-Perez, J. G. “The Early Use of Break-Bone Fever (Quebranta Huesos, 1771) and Dengue (1801) in Spanish.” American Journal of Tropical Medicine and Hygiene, Vol. 59, 1998, pp. 272–274. Rush, A. B. 1789. An Account of the Bilious Remitting Fever, as It Appeared in Philadelphia in the Summer and Autumn of the Year 1780. Philadelphia, PA: Prichard and Hall. “Severe Dengue Infections May Go Unrecognized in International Travelers.” Medical News Today, 1 April 2007. Stephenson, J. R. “Understanding Dengue Pathogenesis: Implications for Vaccine Design.” Bulletin of the World Health Organization, Vol. 83, 2005, pp. 308–314. Stevenson, M. “Spread of Dengue Fever Reaches Fever Pitch in Mexico.” Associated Press, 1 April 2007. “Study: Dengue Fever Is Underreported.” United Press International, 16 October 2007. Thaha, M., et al. “Acute Renal Failure in a Patient with Severe Malaria and Dengue Shock Syndrome.” Clinical Nephrology, Vol. 70, 2008, pp. 427–430. Thammapalo, S., et al. “Relationship between Transmission Intensity and Incidence of Dengue Hemorrhagic Fever in Thailand.” PLoS Neglected Tropical Diseases, Vol. 2, 2008, p. e263. Thoisy, B. D., et al. “Dengue Infection in Neotropical Forest Mammals.” Vectorborne and Zoonotic Diseases, 22 October 2008. Wilder-Smith, A., and J. L. Deen. “Dengue Vaccines for Travelers.” Expert Review of Vaccines, Vol. 7, 2008, pp. 569–578. World Health Organization. “Fact Sheet No. 117: Dengue and Dengue Haemorrhagic Fever.” Revised May 2008. Zhou, H., and M. W. Deem. “Sculpting the Immunological Response to Dengue Fever by Polytopic Vaccination.” Vaccine, Vol. 24, 2006, pp. 2451–2459.

BAD BUGS AND MIRACLE DRUGS Summary of Threat Many disease-causing bacteria are becoming resistant to antibiotics. In addition, many viruses, fungi, parasites, disease vectors (such as mosquitoes), and reservoir hosts (such as rodents) are becoming resistant to the drugs and poisons used to control their numbers. Fighting the war on disease is far more difficult without effective weapons, and the problem is becoming critical.

Other Names Pathogens in this category are popularly called “resistant bugs,” “superbugs,” or “megabugs.” A few of their names are depressingly familiar to the general public, such as MRSA (methicillinresistant Staphylococcus aureus). Many others have names that are familiar only to healthcare workers and undertakers. Table 3.4 lists some of the worst drug-resistant bacteria making the rounds as of 2009.



Table 3.4 Examples of Drug-Resistant Pathogenic Bacteria Species

Name or Strain

Resistant To

Acinetobacter baumannii Acinetobacter baumannii Bacillus anthracis Clostridium difficile Enterobacter sakazakii Enterobacter sakazakii Enterococcus faecium Escherichia coli Escherichia coli Klebsiella pneumoniae Klebsiella pneumoniae Klebsiella pneumoniae Mycobacterium tuberculosis Mycobacterium tuberculosis


Neisseria gonorrhoeae Pseudomonas aeruginosa Pseudomonas aeruginosa Pseudomonas aeruginosa Pseudomonas aeruginosa Pseudomonas aeruginosa Pseudomonas aeruginosa Pseudomonas aeruginosa Salmonella typhi Staphylococcus aureus Stenotrophomonas maltophila Streptococcus pneumoniae Streptococcus pneumoniae


Carbapenem, others MDR + ampicillin/sulbactam Penicillin Metronidazole Imipenem or meropenem Ceftazidime, cefotaxime, or ceftriaxone Vancomycin Ceftazidime, cefotaxime, or ceftriaxone Ciprofloxacin, ofloxacin, or levofloxacin Cephalosporins Imipenem, carbapenem Ceftazidime, cefotaxime, or ceftriaxone Isoniazid, rifampicin Isoniazid, rifampicin, fluoroquinolones + amikacin, kanamycin, or capreomycin Fluoroquinolones Ciprofloxacin Imipenem Ceftazidime Piperacillin Meropenem Ofloxacin Levofloxacin Fluoroquinolones Methicillin Trimethoprim-sulfamethoxazole Cefotaxime or ceftriaxone Penicillin

Sources: World Health Organization (WHO), U.S. Centers for Disease Control and Prevention (CDC).

Description Antibiotics, hailed as “miracle drugs” in the 1940s and 1950s, have become less effective in recent decades due to the evolution of resistant bacteria. Figure 3.5 shows an antibiogram—the result of a laboratory test in which small disks containing antibiotics are placed on a bacterial culture. The antibiotic diffuses from the disk onto the surface of the plate, and if the bacteria grow up to the edge of the disk, they are probably resistant to that antibiotic. Certain resistant bacterial strains have become a major problem in U.S. hospitals, where these bacteria infect an estimated 2 million patients every year. As bacteria evolve, pharmaceutical companies respond by inventing ever more powerful and expensive antibiotics. But bacteria are not the only organisms that have become resistant to common drugs. Many pathogenic viruses, such as HIV, and protozoans, such as the malaria parasite, have shown the same disturbing trend. Governments have stockpiled Tamiflu® in preparation for influenza pandemics, only to discover that many flu viruses are already resistant to it (Chapter 2). Some fungi that cause pneumonia and systemic infections, such as Aspergillus, have also become resistant to antifungal drugs. To make matters worse, the mosquitoes and ticks that vector many diseases are showing increased resistance to DDT and other pesticides. Even the rodents that serve as reservoir hosts



Figure 3.5 Antibiogram study (to measure antibiotic resistance) using a plate culture of the bacterium Enterobacter sakazakii. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

are often resistant to anticoagulants and other common rodenticides. This section, however, will focus mainly on drug-resistant bacteria. In many cases, doctors must resort to potentially dangerous antibiotics because the safer ones no longer work. In other cases, no drug is effective, and doctors find themselves in the same situation they faced a century ago, watching helplessly as patients die of untreatable infections. Resistant bacteria that infect wounds or cause pneumonia have emerged as perhaps the most deadly long-term biological threat we face today.

Who Is at Risk? Antibiotic resistance represents a threat to everyone. As usual, the most vulnerable groups are the very young, the very old, the poor and malnourished, and those with suppressed immune systems. Since studies have shown that infection rates vary widely from one hospital to another, living near a bad hospital might be the most important risk factor of all. Unfortunately, communityacquired drug-resistant infections (those acquired outside hospitals) are also becoming common. In one study, poultry workers were 32 times as likely as others to carry gentamicin-resistant E. coli. Pig farmers are reportedly at risk for MRSA (Figure 3.6). People who buy herbal supplements from health food stores represent another, less expected risk group. According to a 2008 study, potentially dangerous antibiotic-resistant bacteria (including the famous Stenotrophomonas maltophila) were present in samples of several herbal products. Football players are at risk for MRSA, apparently because of injuries and shared equipment.



Figure 3.6 Scanning electron micrograph showing clumps of a methicillin-resistant strain (MRSA) of the bacterium Staphylococcus aureus. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

The Numbers Every year, an estimated 2 million Americans acquire bacterial infections while hospitalized, and about 100,000 die as a result. One of the worst offenders is Clostridium difficile, a bacterium that causes diarrhea and is resistant to most known antibiotics. It infects some 300,000 hospitalized patients in the United States annually, and an estimated 1 in every 1,000 patients in Europe— but the death rate was low until about 2006, when a highly virulent strain began to emerge. As a result, C. difficile did not even make the “top six” in a 2006 report by the Infectious Diseases Society of America: 1. Acinetobacter baumanni first gained public attention because of infections in soldiers returning from Iraq—between 2002 and 2004. It now accounts for about 7 percent of all hospital-acquired cases of bacterial pneumonia in the United States, and it is resistant to most drugs. Reported mortality rates range from 19 to 54 percent. 2. Aspergillus is a fungus that often infects people with compromised immune systems, but it was already a killer when AIDS was unknown. In 1978–1982, for example, it caused 1 in every 200 hospital deaths in Germany. Drug-resistant strains emerged in about 1990, and the death rate now exceeds 50 percent. 3. Methicillin-resistant Staphylococcus aureus (MRSA) infected about 880,000 hospital patients in 2007, and it is also common in community-acquired infections. It can survive for up to 12 days on contaminated surfaces. In 2005, about 18,650 Americans died from



MRSA (and 16,000 from AIDS). In 2008, Targanta reported that a new antibiotic called oritavancin was effective against MRSA, at least temporarily. 4. ESBL-producing bacteria (which produce the enzyme extended-spectrum beta lactamase, or ESBL) as a group are resistant to antibiotics called cephalosporins. The two most common examples, E. coli and Klebsiella, cause thousands of urinary tract and wound infections every year, with mortality as high as 64 percent. 5. Vancomycin-resistant Enterococcus faecium (VRE) is a major cause of bloodstream infections, meningitis, and endocarditis in hospital patients. In a 2006 survey, 10 percent of patients harbored this bacterium, which is resistant to most antibiotics. Some hospitals reportedly refuse to admit patients with this infection. 6. The bacterium Pseudomonas aeruginosa is particularly dangerous for patients with HIV or cystic fibrosis, because it can quickly become resistant to any antibiotic. In some cases, the only available treatment is a lung transplant.

History Scottish scientist Alexander Fleming discovered penicillin in 1928, and German chemists created the first sulfa drugs in 1932. Other “miracle drugs” followed in rapid succession. When these drugs first appeared, doctors and the general public tended to use them indiscriminately. But whenever populations of living organisms are exposed to a poison, resistance is likely to evolve. Some bacteria, for example, have genes that enable them to produce enzymes (such as ESBL) that break down the antibiotic molecule. Bacteria with this capability are more likely than others to survive and reproduce in the presence of antibiotics. Some antibiotic-resistant bacteria can even transfer the resistance genes to other species of bacteria. As a result, many bacterial infections that were once treatable are now resistant. But it would not be fair to blame medical science; the first doctors who used antibiotics were simply trying to save lives. Parents must also accept their share of responsibility, for demanding antibiotics every time their child has the sniffles. Some survivalist groups encourage their members to stockpile antibiotics that they have no idea how to use, while other people reportedly take antibiotics for their anti-inflammatory effect. All these are minor players compared with factory farms, which use antibiotics to prevent disease outbreaks and promote growth in livestock. In the early twentyfirst century, such farms use about 70 percent of all antibiotics in the United States.

Prevention and Treatment If the entire patient population converged on a few excellent hospitals (such as Johns Hopkins in Baltimore) to avoid infection with superbugs, the healthcare system would soon collapse. Alternatively, perhaps the state and federal agencies that regulate hospitals could simply do a better job of enforcing sanitation requirements. New methods of disinfection might help if consistently applied; for example, a recent study showed that a specific wavelength of blue light can kill MRSA on hospital surfaces. Pharmaceutical companies are in the process of developing more effective antibiotics, but there are obstacles. Companies need to earn a profit, and the return on investment is reportedly low for anti-infective drugs in general. There is also the age-old dance of predator and prey; as soon as a new antibiotic is invented and bacteria encounter it, resistance is likely to evolve (Case Study 3-7). Another approach would focus on convenient, affordable tests that would enable doctors to distinguish between bacterial and viral infections. Studies have shown that communities



Case Study 3-7: Back to the Drawing Board Villagers in the South American nation of Guyana (famous for the 1978 Jonestown incident) have used the drug chloroquine for many years to prevent and treat malaria. The unexpected result is that most of these people now harbor E. coli and other bacteria that are resistant to the antibiotic ciprofloxacin. Why? It turns out that cipro is chemically related to chloroquine, although the latter is not an antibiotic. Thus, bacteria exposed to chloroquine also become resistant to cipro. Doctors have always assumed that there was no interaction between treatments used for bacterial and parasitic infections, but that assumption clearly was wrong. Fortunately, bacterial resistance is often reversible. As soon as an effective malaria vaccine becomes widely available, the use of chloroquine will probably decline.

can reduce the prevalence of resistant bacteria by avoiding the unnecessary use of antibiotics. For example, in Finland in the 1990s, concerns about erythromycin-resistant Streptococcus A led to a campaign to reduce erythromycin use. The result was a reduction in resistance levels from 19 percent to 9 percent in only three years. Yet another approach to defeating enteric superbugs is the fecal transplant. This procedure is exactly what it sounds like. The physician obtains a sample of fecal material from a healthy person and injects it into the colon of a person infected with Clostridium difficile. Despite aesthetic problems, the reported success rate is as high as 90 percent.

Popular Culture

In 2007, fans of the TV series Project Runway were shocked to learn that a participant was receiving hospital treatment for a life-threatening MRSA infection. This one incident probably generated more public controversy and concern than all the hundreds of thousands of similar infections that afflict U.S. residents every year. Robin Cook’s 2007 novel Critical explores the personal and economic impacts of a devastating MRSA epidemic at three New York hospitals. The characters include a conflicted physician turned CEO, dastardly Mafiosos, and a pathologist whose husband needs knee surgery. Giving away the ending would be just wrong. In the 2004 motion picture The Day after Tomorrow, a young woman in flooded Manhattan cuts her leg on submerged debris and develops a severe bacterial infection. She recovers quickly after a single shot of penicillin, but in real life she might not be so lucky. Similar wound infections that occurred in the wake of Hurricane Katrina were fatal in about 50 percent of cases, and were mostly resistant to penicillin. In the 1958 motion picture Earth versus the Spider, a really large spider goes on a killing rampage until the bad sheriff’s minions squirt it with DDT. The spider is stunned at first, but unexpectedly recovers, and the hero ends up electrocuting it instead. Scientists already knew about DDT resistance in the 1950s, but people were so busy congratulating themselves on the chemical defeat of malaria that they tended not to listen. (Unfortunately, electric bug zappers have not lived up to expectations either.) For the origin of “Bugzilla,” see Case Study 3-8.

The Future New drugs to prevent (rather than cure) resistant bacterial infection would help. In 2008, researchers were conducting human trials of a bacteriocidal gel that can be applied to the nostrils. New classes of antibiotics may also be on the horizon, but bacteria will probably become resistant


to these drugs as well. Another approach is the use of designer probiotics—genetically engineered bacteria that attack pathogens. Again, the pathogens will undoubtedly fight back. Also, there is no scientific advance that cannot be turned to mischief. The same technologies that give us designer drugs and bugs may enable terrorists to create drug-resistant pathogens.

References and Recommended Reading


Case Study 3-8: Superbug Hype Real superbugs are bad enough, but exaggerated ones are worse. In 2008, the press christened the opportunistic bacterium Stenotrophomonas maltophila “the megabug” or “Bugzilla” and hinted darkly at mass casualties. To put the matter in perspective, S. maltophila was responsible for less than 1 percent of all reported bloodstream infections in 2007. It does not appear to spread easily between patients, and in 2008 it remained treatable with at least one antibiotic. The misunderstanding apparently started when researchers published a description of the S. maltophila genome and referred to its “remarkable capacity for drug and heavy metal resistance.” Scientists and science writers need to choose words carefully.

Adler, J., and J. Interlandi. “Caution: Killing Germs May Be Hazardous to Your Health.” Newsweek, 29 October 2007. Blakeslee, H. W. “Some Germs Sneer at Sulfa.” Daily Capital News, 5 August 1943. “Blue Light Destroys MRSA.” United Press International, 30 January 2009. Coates, A. R., and Y. Hu. “Novel Approaches to Developing New Antibiotics for Bacterial Infections.” British Journal of Pharmacology, Vol. 152, 2007, pp. 1147–1154. Croft, A., et al. “Update on the Antibacterial Resistance Crisis.” Medical Science Monitor, Vol. 13, 2007, pp. RA103–RA118. Datta, R., and S. S. Huang. “Risk of Infection and Death Due to Methicillin-Resistant Staphylococcus aureus in Long-Term Carriers.” Clinical Infectious Diseases, Vol. 47, 2008, pp. 176–81. Donnellan, E. “Dangers of Antibiotic Overuse Highlighted.” Irish Times, 18 November 2008. Engel, M. “Proposal Targets a Deadly Infection.” Los Angeles Times, 1 January 2008. “Experts Concerned about Flu, MRSA Combo.” United Press International, 27 April 2008. “Flies May Be Spreading MRSA from Fowl Feces.” Reuters, 16 March 2009. Goldburg, R., et al. “The Risks of Pigging Out on Antibiotics.” Science, Vol. 321, 2008, p. 1294. Gould, I. M. “The Epidemiology of Antibiotic Resistance.” International Journal of Antimicrobial Agents, 29 August 2008. Groopman, J. “Superbugs.” The New Yorker, 11 August 2008. Gulshan, K., and W. S. Moye-Rowley. “Multidrug Resistance in Fungi.” Eukaryotic Cell, Vol. 6, 2007, pp. 1933–1942. Hawkey, P.M. “The Growing Burden of Antimicrobial Resistance.” Journal of Antimicrobial Chemotherapy, Vol. 62, Supplement 1, 2008, pp. 1–9. Hellemans, R., et al. “Fecal Transplantation for Recurrent Clostridium difficile Colitis, an Underused Treatment Modality.” Acta Gastro-Enterologica Belgica, Vol. 72, 2009, pp. 269–270. “Influenza A Showing Tamiflu Resistance.” United Press International, 19 December 2008. Ishizuka, M., et al. “Pesticide Resistance in Wild Mammals—Mechanisms of Anticoagulant Resistance in Wild Mammals.” Journal of Toxicological Sciences, Vol. 33, 2008, pp. 283–91. Johnson, A. P., and G. J. Duckworth. “The Emergence of Stenotrophomonas maltophila.” British Medical Journal, Vol. 336, 2008, p. 1322. Juncosa, B. “Antibiotic Resistance: Blame It On Livesaving Malaria Drug?” Scientific American, 21 July 2008. Kuchment, A. “Trapping the Superbugs.” Newsweek, 13 December 2004. Larson, E. “Community Factors in the Development of Antibiotic Resistance.” Annual Review of Public Health, Vol. 28, 2007, pp. 435–447. Linares, J. F., et al. “Antibiotics as Intermicrobial Signaling Agents Instead of Weapons.” Proceedings of the National Academy of Sciences (U.S.), Vol. 103, 2006, pp. 19484–19489. Merpol, S. B. “Valuing Reduced Antibiotic Use for Pediatric Acute Otitis Media.” Pediatrics, Vol. 121, 2008, pp. 669–673.



“New Test Shows Promise at Reducing Antibiotic Use.” Associated Press, 18 February 2004. “Out of Patience with Hospital Infections.” United Press International, 24 July 2008. Ozolins, M., et al. “Comparison of Five Antimicrobial Regimens for Treatment of Mild to Moderate Inflammatory Facial Acne Vulgaris in the Community: Randomised Controlled Trial.” Lancet, Vol. 364, 2004, pp. 2188–2195. Park, A. 2007. “Fighting Drug-Resistant Bugs.” Time, 7 June 2007. Patrick, D. M. “Antibiotic Use and Population Ecology: How You Can Reduce Your ‘Resistance Footprint.’” Canadian Medical Association Journal, Vol. 180, 2009, pp. 416–421. “Possible MRSA Cure Undergoing Trials.” United Press International, 18 May 2008. “Powerful Antibiotic Battles MRSA.” United Press International, 22 October 2008. Roberts, D. R., and R. G. Andre. “Insecticide Resistance Issues in Vector-Borne Disease Control.” American Journal of Tropical Medicine and Hygiene, Vol. 50 (6 Suppl.), 1994, pp. 21–34. Roghmann, M. C., and L. McGrail. “Novel Ways of Preventing Antibiotic-Resistant Infections: What Might the Future Hold?” American Journal of Infection Control, Vol. 34, 2006, pp. 469–475. Rubinstein, E., et al. “Pneumonia Caused by Methicillin-Resistant Staphylococcus aureus.” Clinical Infectious Diseases, Vol. 46, Supplement 5, 2008, pp. S378–S385. Sachs, J. “The Superbugs Are Here.” Prevention, December 2006. Santamour, B. “As a Superbug Spreads, So Does Misinformation.” Hospitals and Health Networks, Vol. 82, 2008, pp. 36–40. Seppälä, H., et al. “The Effect of Changes in the Consumption of Macrolide Antibiotics on Erythromycin Resistance in Group A Streptococci in Finland.” New England Journal of Medicine, Vol. 337, 1997, pp. 441–446. Sleator, R. D., and C. Hill. “Battle of the Bugs.” Science, Vol. 321, 2008, pp. 1294–1295. Stobbe, M. “Gut Superbug Causing More Illnesses, Deaths.” Associated Press, 28 May 2008. Talbot, G. H., et al. “Bad Bugs Need Drugs: An Update on the Development Pipeline from the Antimicrobial Availability Task Force of the Infectious Diseases Society of America.” Clinical Infectious Diseases, Vol. 42, 2006, pp. 657–668. Ward, T. “Spread of MRSA: Past Time for Action.” Medscape Journal of Medicine, Vol. 10, 2008, p. 32. “Yeast May Combat Antibiotic-Resistant Pneumonia and Malaria.” News Release, Dartmouth-Hitchcock Medical Center, 21 January 2004.

EMERGING DISEASES Summary of Threat An emerging disease is one that has recently appeared in a population for the first time, or one that previously existed but is rapidly increasing in incidence or geographic range. These diseases tend to be media favorites, because they are unfamiliar to most people and therefore frightening. This section will examine seven examples: SARS, West Nile, Ebola, Lyme disease, “pig strep,” the arenaviruses, and diphtheria.

Other Names Diphtheria is a re-emerging disease that humans have known and dreaded for centuries. Its older names include Bretonneau’s disease, angina diphtherica, and diphtheritic malignant angina. The agent was formerly called the Krebs-Loeffler bacillus. The other six examples are too new or unfamiliar to have acquired many names. SARS (severe acute respiratory syndrome) has no other English name as of 2009. West Nile virus is commonly called WNV. Ebola has four isolates called Ebola Reston, Ebola Sudan, Ebola Zaire,



and Ebola Tai; “green monkey disease” refers to the closely related Marburg virus. Lyme disease is often called Lyme borreliosis. Pig strep is human infection with the swine bacterium Streptococcus suis. Arenaviruses include the agents of lymphocytic choriomeningitis (LCM), Lassa fever, and other diseases.

Description The first known cases of severe acute respiratory syndrome (SARS) in 2003 started with a high fever, headache, and cough that rapidly progressed to severe pneumonia with a high fatality rate (10 to 20 percent). Many patients also had diarrhea. The virus (Figure 3.7) spread by contact

Figure 3.7 Electron micrograph showing a coronavirus identified as the cause of the 2003 SARS outbreak in Asia. Source: Swedish Institute for Infectious Disease Control.



with contaminated surfaces and also by airborne transmission. A 2004 study determined that aerosol droplets from a flushed toilet transmitted the disease to residents of an apartment building in Hong Kong. West Nile Virus (WNV) is just one of several forms of mosquito-borne viral encephalitis, and not the most deadly. It is famous because of its abrupt arrival in New York in 1999 and its rapid invasion of all 48 conterminous states. Most infected people have no symptoms or only a mild illness. Severe cases (less than 1 percent) may cause convulsions, paralysis, or coma, but the death rate for hospitalized patients is below 4 percent. Long-term effects, if any, may include polio-like limb weakness. WNV also infects horses, dogs, cats, and a number of wild mammals and birds. Ebola hemorrhagic fever has been the darling of shock journalists since its 1976 discovery in Zaire (now called the Democratic Republic of the Congo). Symptoms include a high fever, headache, vomiting, and diarrhea, often followed by bleeding from every orifice, multiple organ failure, and death. The agent is a filovirus (Figure 3.8), similar to those that cause some other hemorrhagic fevers. Fruit bats apparently serve as reservoir hosts. Lyme disease has achieved a high level of public awareness in the United States, although the death rate is near zero. The agent is a spirochete, and the clinical course is comparable to that of syphilis. But Lyme does not spread directly from one person to another; it is transmitted by ticks, specifically the immature stages of certain deer ticks. Early symptoms often include fever, joint pain, and the famous bulls-eye rash (Figure 3.9). Long-term effects of Lyme are controversial.

Figure 3.8 Transmission electron micrograph showing the virus that causes Ebola hemorrhagic fever. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

Figure 3.9 Typical “bull’s-eye” rash of Lyme disease. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



Figure 3.10 Transmission electron micrograph showing a recently discovered arenavirus that can cause fatal hemorrhagic fever in humans. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

The bacterium Streptococcus suis mainly infects pigs and other domesticated animals. In recent years, however, pig strep has caused outbreaks among swine workers in China, southeast Asia, and Europe. Many people in North America are at risk, but only sporadic human cases have been reported. Pig strep can cause hemorrhagic fever, meningitis, septicemia, arthritis, or endocarditis. Arenaviruses include the agents of Lassa fever, lymphocytic choriomeningitis, Argentine hemorrhagic fever, and several other diseases (Figure 3.10). Most cause the proverbial flu-like symptoms followed by neurological signs; some also cause bleeding, and at least one (LCM) can cause miscarriage or birth defects. Arenaviruses spread directly between humans by airborne droplet, from mother to fetus, or by organ transplantation. Some outbreaks appear to be associated with wild rodents. There is no nonpolitical reason for anyone to have diphtheria nowadays, because the vaccine has been available for nearly a century, and it is highly effective and cheap. The agent, a bacterium called Corynebacterium diphtheriae, produces its deadly toxin only if a phage (a virus that reproduces in bacteria) is present. Diphtheria usually affects the tonsils and throat and can cause death by asphyxiation. It can also infect the skin (Figure 3.11).

Who Is at Risk? The only known risk factor for SARS is exposure to people with SARS, or possibly exposure to infected fruit bats. As of 2009, no country has reported SARS for the past five years, but it would be a mistake to assume that the disease no longer exists.



Figure 3.11 A diphtheria skin lesion on a human leg. Once nearly eradicated in most of the world, diphtheria is now a re-emerging disease Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

Mosquitoes transmit West Nile virus, and people who work or live outdoors are at increased risk of being bitten (Case Study 3-9). Risk factors for severe disease include old age, high blood pressure, diabetes, and immune suppression. Thanks to an overzealous press, many people think they are at risk for Ebola. In fact, it seems to be a difficult disease to catch, even in endemic areas. Visitors to Africa should avoid obvious hazards such as handling dead animals. In 2009, an American visiting Uganda contracted the closely related Marburg virus after touring a cave occupied by fruit bats. (He recovered, and none of his contacts became ill.) People who do not check themselves carefully for ticks after walking in the woods are most likely to be at risk for Lyme disease. An immature deer tick is extremely small and easy to miss (see Figure 6.6, page 239). Parents should teach children how to check for ticks and how to remove them safely.

Case Study 3-9: West Nile and the Homeless The arrival of West Nile in North America added one more item to the list of biohazards facing the homeless community. Without window screens (or windows), the homeless cannot avoid exposure to mosquitoes. A 2007 study of nearly 400 homeless people in Houston, Texas, showed that about 7 percent had been infected with West Nile. Those who spent most of their time outdoors due to less stable housing arrangements were at greatest risk, with seroprevalence of about 13 percent. Other studies have confirmed this finding. Unexpectedly, subjects in the 2007 study who used mosquito precautions were more likely than others to be infected, possibly because the precautions available to them (such as candles or swatting) were ineffective.



The only known risk factor for pig strep is exposure to sick pigs, goats, or other livestock. Breaks in the skin may increase risk. A 2008 In the winter of 1925 a diphtheria epidemic study showed that nearly 10 percent of Iowa was raging in Nome, Alaska. To save the swine workers were seropositive for pig strep, town, a relay team of ten dogsled drivers but none of them had developed clinical illness. transported a supply of diphtheria antitoxin As of 2009, there are no reports of direct trans674 miles through blizzards that made air travel impossible. Edgar Nollner drove the mission from one human to another. last leg of the dog relay and delivered the As of 2009, the risk factors for arenavirus serum in record time. Mr. Nollner died in diseases are poorly understood, but may 1999 at age 94, survived by 20 children and include contact with the feces or urine of wild an estimated 200 grandchildren. A widely or domesticated rodents. Some cases of lymheld belief—recently repeated on the Hisphocytic choriomeningitis have been traced to tory Channel—is that the annual Iditarod pet hamsters, house mice, or other rodents. race commemorates the 1925 serum run. Lassa fever is unknown outside Africa, where Other sources claim that the purpose of the the incidence is highest during the dry season. race (established in 1967) was to commemoOther arenaviruses occur in North and South rate the 1909 Alaskan gold rush or the 1908 America. All Alaskan Sweepstakes Race. The purpose of today’s Iditarod is a matter of conjecture, Unvaccinated persons are at risk during but 1967 newspaper articles about the first diphtheria outbreaks, which usually occur race do not mention the serum run. either in isolated populations (Case Study 3-10), in groups that oppose vaccination, or in countries where political instability has disrupted the healthcare system. Older people may need booster shots. Case Study 3-10: An Alaskan Hero

The Numbers According to WHO, the 2003–2004 SARS outbreak caused 8,450 reported cases (from 29 countries) and 810 deaths. Thus, the death rate was nearly 10 percent. In 2007, the United States had about 35,000 reported cases of West Nile (1,227 of them serious) and 117 reported deaths. The statistics for other years have been similar, but the mortality rate is hard to determine because many mild cases are undetected. As of 2009, the largest Ebola outbreak to date was in Uganda in 2000–2001, with 425 reported cases and 224 deaths (53 percent). Other outbreaks have ranged in size from a few cases to a few hundred, with mortality rates of 25 to 90 percent. In 2006, the CDC reported nearly 20,000 new cases of Lyme disease in the United States. The incidence doubled between 1991 (when Lyme became a notifiable disease) and 2007. Some sources attribute the increase to rising deer populations (Chapter 6); others think the numbers are inflated, due to media coverage and inaccurate testing; others claim that Lyme is underreported due to a lack of public awareness. During the 2005 pig strep outbreak in China, there were 215 human cases and 38 deaths (about 18 percent). The death rate was highest among those who developed toxic shock syndrome. Case fatality rates for arenavirus infections range from about 5 percent to over 30 percent, depending on the specific virus and the form of the infection. The former Soviet Union had a major resurgence of diphtheria in 1990–1996, apparently because of the breakdown of healthcare services, with some 150,000 cases and 5,000 deaths. If these numbers are accurate, the death rate was about 3 percent. In 1921, by comparison, the United States had about 200,000 cases of diphtheria, with death rates of 5 percent to 10 percent depending on the age group.



History A Chinese cook who prepared wild animal dishes may have started the SARS epidemic in 2002, but one hopes that his name will not join Mrs. O’Leary’s cow and AIDS “Patient Zero” on history’s scapegoat roster. SARS spread from China to other Asian countries and eventually to Canada, causing global panic and various measures that later proved ineffective, such as the wholesale slaughter of civet cats (a suspected reservoir host). But no new cases appeared after April 2004, and as of 2009 the disease has not returned. The rapid identification of the SARS coronavirus, by laboratories in three countries working in cooperation, ranks among the greatest of public health achievements. First discovered in Uganda in 1937, West Nile made its debut in New York in 1999. Some people blamed its arrival on global warming, others on terrorism; it was more likely the usual story of risks and benefits from international travel. Within a few years, the range of WNV included most of North America and part of South America. Human cases in Mexico have been rare, although Mexican horses have contracted the disease. The first official Ebola outbreaks occurred in Zaire and Sudan in 1976–1977. A small outbreak in Sudan followed in 1979, but except for a series of highly publicized laboratory accidents (in the Philippines and the United States), Ebola did not resurface until the 1990s. The high mortality rate and dramatic symptoms have made Ebola a greatly feared disease. European doctors described a disease similar to Lyme before 1900 and associated it with tick bites in 1909. The disease did not receive a name until 1975, after an outbreak of juvenile rheumatoid arthritis in the town of Lyme, Connecticut. A 2005 disease outbreak in China inspired international rumors of a virulent new strain of bird flu, dengue hemorrhagic fever, or even Ebola. The world had not forgotten SARS. But the hysteria subsided when the agent was identified as the well-known bacterium Streptococcus suis. Sporadic human cases had previously occurred in Asia and Europe; the first human cases in North America appeared in 2006. Researchers studying St. Louis encephalitis in 1933 discovered the first known arenavirus (LCM) by accident. Since then, new arenaviruses have turned up every few years. These viruses tend to cause small outbreaks, often associated with rodents. For example, the Whitewater Arroyo virus caused fatal hemorrhagic fever in three California women in 1999–2000. Woodrats (Neotoma) apparently serve as a reservoir host for this arenavirus, but the specific circumstances of transmission are unclear. During the nineteenth century, diphtheria claimed the lives of several thousand American children every year. The history of diphtheria should have ended when the vaccine became available in the 1920s, but this disease tends to return whenever public health programs falter. The largest recent epidemic was in the former Soviet Union, as previously discussed.

Prevention and Treatment Doctors in 2003–2004 found no effective treatment for SARS. Steroids and antiviral drugs proved ineffective. The best preventive measures were among the oldest: quarantine and protective masks. According to a 2003 report, healthcare personnel wearing surgical masks or N95 particle respirator masks were 13 times less likely to contract SARS than those without masks. As of 2009, there is no West Nile vaccine approved for human use in the United States, but there is one for horses. The best preventive measure is to avoid mosquito bites, by wearing mosquito repellent, and by making sure all windows have intact screens.



Experimental Ebola vaccines have been effective in laboratory animals, but as of 2009, treatment of infected human patients focuses on supportive care (see also Case Study 7-15, page 282). Males who recover are advised to avoid sexual relations until semen is free of virus. GlaxoSmithKline introduced a Lyme disease vaccine in 1999 and pulled it off the market in 2002, citing low demand and poor sales. According to a 2006 Nature editorial, the withdrawal of this vaccine was a prime example of “unfounded public fears” blocking vaccine development. Oral antibiotics usually cure Lyme disease, but only if given within a few days after a tick bite, and only if the person really has Lyme. Chinese officials reportedly stopped the 2005 Streptococcus suis outbreak by prohibiting “backyard slaughtering.” Workers in commercial slaughterhouses wore protective clothing that was not available to most infected farmers. Some arenavirus infections are treatable with ribavirin. Pet rodents should not be allowed to hang out with wild rodents. Pregnant women should wear gloves and masks when handling rodents or, better yet, avoid handling them at all. Doctors usually administer diphtheria vaccine to children in a trivalent vaccine called DTaP (diphtheria and tetanus toxoids and acellular pertussis). An older, less expensive version called DPT is also in use. An unvaccinated person who is exposed to diphtheria should receive diphtheria antitoxin as soon as possible, followed by antibiotics if necessary. Popular Culture In the 1995 movie Outbreak, an Ebola-like viral disease becomes airborne and infects a town. Such an outbreak might happen, but it’s highly unlikely that two Army doctors could whip up an effective antiserum in a few hours and quickly restore people to full health from the end stage of multiple organ failure. Modern parents who oppose vaccination might wish to read Stewart O’Nan’s 1999 novel A Prayer for the Dying, which deals with the horrors of a diphtheria epidemic in Wisconsin after the Civil War. In 2007, a television program aired the theory that the Jersey Devil—a legendary creature of the Mid-Atlantic states—might be a hammer-headed fruit bat that escaped from the Plum Island Animal Disease Center. This large bat is a host for the Ebola virus in Africa, and it would certainly scare the daylights out of any inebriated duck hunter who came upon it in the New Jersey woods. But—(The author was about to divulge the true identity of the Jersey Devil, when three visitors in black suits warned her to keep quiet.) In his 1842 short story “The Masque of the Red Death,” Edgar Allen Poe described a fictitious but seemingly Ebola-like disease: The ‘Red Death’ had long devastated the country. No pestilence had ever been so fatal, or so hideous. Blood was its Avatar and its seal—the redness and the horror of blood. There were sharp pains, and sudden dizziness, and then profuse bleeding at the pores, with dissolution. The scarlet stains upon the body and especially upon the face of the victim, were the pest ban which shut him out from the aid and from the sympathy of his fellow-men. And the whole seizure, progress and termination of the disease, were the incidents of half an hour.1

Did Poe foresee Ebola? Or has a similar disease surfaced in the past, leaving a vivid collective memory? Did Ebola, like pizza and the Internet, come along and fill a vacant niche in the human soul? To paraphrase a familiar quotation: if Ebola did not exist, would mankind have felt obliged to invent it? Edgar Allen Poe apparently did. 1. E. A. Poe, Short Stories (NY: Editions for the Armed Services, 1945).



The Future According to several infectious disease experts quoted in a 2009 report, the global recession could hasten the spread of exotic diseases by interfering with vector control and surveillance programs. By the time this book is published, perhaps we will know whether they were right or not. The study of global climate change (Chapter 6) is another perennial source of emerging disease warnings.

References and Recommended Reading Amman, B. R., et al. “Pet Rodents and Fatal Lymphocytic Choriomeningitis in Transplant Patients.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 719–725. Badiaga, S., et al. “Preventing and Controlling Emerging and Reemerging Transmissible Diseases in the Homeless.” Emerging Infectious Diseases, Vol. 14, 2008, pp. 1353–1359. Bausch, D. G., et al. “Treatment of Marburg and Ebola Hemorrhagic Fevers: A Strategy for Testing New Drugs and Vaccines under Outbreak Conditions.” Antiviral Research, Vol. 78, 2008, pp. 150–161. Chastel, C. “Global Threats from Emerging Viral Diseases.” Bulletin de l’Académie Nationale de Médecine, Vol. 191, 2007, pp. 1563–1577. [French] Choi, C.Q. “Going to Bat: Natural Reservoir for Emerging Viruses May Be Bats.” Scientific American, March 2006, pp. 24–24B. Dong, J., et al. “Emerging Pathogens: Challenges and Successes of Molecular Diagnostics.” Journal of Molecular Diagnostics, Vol. 10, 2008, pp. 185–197. Enserink, M. “New Arenavirus Blamed for Recent Deaths in California.” Science, Vol. 289, 2000, pp. 842–843. European Centre of Disease Prevention and Control. “Arenaviruses—Factsheet.” Updated 14 October 2008. “First U.S. Case of Marburg Fever Confirmed.” Associated Press, 8 February 2009. Gonzalez, J. P., et al. “Arenaviruses.” Current Topics in Microbiology and Immunology, Vol. 315, 2007, pp. 253–288. Gonzalez, J. P., et al. “Ebolavirus and Other Filoviruses.” Current Topics in Microbiology and Immunology, Vol. 315, 2007, pp. 363–387. Jamieson, D. J., et al. 2006. “Lymphocytic Choriomeningitis Virus: an Emerging Obstetric Pathogen?” American Journal of Obstetrics and Gynecology, Vol. 194, 2006, pp. 1532–1536. Knobler, S., et al. (Eds.) 2004. Learning from SARS: Preparing for the Next Disease Outbreak. Washington, D.C.: National Academies Press. Le Guenno, B. “Haemorrhagic Fevers and Ecological Perturbations.” Archives of Virology Supplement 13, 1997, pp. 191–199. Lee, G. T., et al. “Streptococcus suis Meningitis, United States.” Emerging Infectious Diseases, Vol. 14, 2008, pp. 183–185. Lemonick, M. D. “A Deadly Mystery.” Time, 26 April 2007. Leroy, E. M., et al. “Fruit Bats as Reservoirs of Ebola Virus.” Nature, Vol. 438, 2005, pp. 575–576. Lindsey, N. P., et al. “West Nile Virus Activity—United States, 2007.” Morbidity and Mortality Weekly Report, Vol. 57, 2008, pp. 720–723. Loeb, M., et al. “Prognosis After West Nile Virus Infection.” Annals of Internal Medicine, Vol. 149, 2008, pp. 232–241. Meyer, T. E., et al. “West Nile Virus Infection Among the Homeless, Houston, Texas.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1500–1503. Motavelli, J. “Connecting the Dots: the Emerging Science of Conservation Medicine Links Human and Animal Health with the Environment.” E: The Environmental Magazine, November–December 2004. Nakazibwe, C. “Marburg Fever Outbreak Leads Scientists to Suspected Disease Reservoir.” Bulletin of the World Health Organization, Vol. 85, 2007, pp. 654–656. Oglesby, C. “West Nile Virus a North American Fixture.” CNN, 6 June 2005. Oldstone, M. B. “A Suspenseful Game of “Hide and Seek” between Virus and Host.” Nature Immunology, Vol. 8, 2007, pp. 325–327. Omi, S. 2006. SARS: How a Global Epidemic Was Stopped. Geneva: World Health Organization.



Osterhaus, A. D. M. E., et al. “The Aetiology of SARS: Koch’s Postulates Fulfilled.” Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, Vol. 359, 2004, pp. 1081–1082. Peters, C. J. “Emerging Infections: Lessons from the Viral Hemorrhagic Fevers.” Transactions of the American Clinical and Climatological Association, Vol. 117, 2006, pp. 189–197. Qiu, W.-G., et al. “Wide Distribution of a High-Virulence Borrelia burgdorferi Clone in Europe and North America.” Emerging Infectious Diseases, Vol. 14, 2008, pp. 1097–1104. “Scientists Develop SARS Vaccine.” United Press International, 19 July 2006. Skovgaard, N. “New Trends in Emerging Pathogens.” International Journal of Food Microbiology, Vol. 120, 2007, pp. 217–224. Snelson, H. “PRRS and Ebola Virus Reported in Philippine Pigs.” News Release, American Association of Swine Veterinarians, 15 December 2008. “Study: Bats, Not Civets, Source of SARS.” United Press International, 20 February 2008. Reilley, B., et al. “SARS and Carol Urbani.” New England Journal of Medicine, Vol. 348, 2003, pp. 1951–1952. “Russian Scientist Dies of Ebola after Lab Accident.” CIDRAP News, 25 May 2004. Schnirring, L. 2008. “Tests Indicate an Arenavirus in South African Deaths.” CIDRAP News, 13 October 2008. Shapiro, E. D. 2008. “Lyme Disease.” Advances in Experimental Medicine and Biology, Vol. 609, 2008, pp. 185–195. Thomas, R. M. “Edgar Nollner, 94, Dies; Hero in Epidemic.” New York Times, 24 January 1999. U.S. Centers for Disease Control and Prevention. “Fact Sheet: Basic Information About SARS,” 13 January 2004. U.S. Centers for Disease Control and Prevention. “Brief Report: Lymphocytic Choriomeningitis Virus Transmitted through Solid Organ Transplantation—Massachusetts, 2008.” Morbidity and Mortality Weekly Report, Vol. 57, 2008, pp. 799–801. U.S. Centers for Disease Control and Prevention. “Fact Sheet: Lymphocytic Choriomeningitis” (undated). University of California, Berkeley. “Arenavirus Infection Linked to Deaths in California.” Media release, 4 August 2000. Wang, L. F., and B. T. Eaton. “Bats, Civets and the Emergence of SARS.” Current Topics in Microbiology and Immunology, Vol. 315, 2007, pp. 325–344. Weinstein, R. A. “Planning for Epidemics—the Lessons of SARS.” New England Journal of Medicine, Vol. 350, 2004, pp. 2332–2334. Weiss, R. A., and A. J. McMichael. “Social and Environmental Risk Factors in the Emergence of Infectious Diseases.” Nature Medicine, Vol. 10 (Suppl. 12), 2004, pp. S70–S76.

WHAT ABOUT PNEUMONIA? Summary of Threat Pneumonia is a major cause of death worldwide, but it is not a single disease. Many infectious diseases (including most of those described in this book) can result in pneumonia, defined as inflammation and consolidation in one or both lungs. In fatal cases of measles and influenza, the cause of death is often secondary pneumonia. Other diseases and some chemical exposures can cause primary pneumonia. Other Names Pneumonia with inflammation of the bronchi is called bronchopneumonia. Lobar pneumonia is bacterial pneumonia that involves only one lobe of a lung. So-called walking pneumonia is a



just a mild case of pneumonia, often caused by Mycoplasma; but the similarly named wandering pneumonia is an infection that invades successive parts of the lung. Aspiration pneumonia results from inhalation of food, vomit, or other material. The terms organizing pneumonia and organized pneumonia refer to the presence of fibrous tissue in the alveoli. When the bronchioles are also affected, the condition is bronchiolitis obliterans organizing pneumonia (BOOP). Specific forms of pneumonia bear the names of their agents, such as pneumococcal, chlamydial, or PC (Pneumocystis carinii) pneumonia. Older names for pneumonia include winter fever, lung fever, and old man’s friend. Most names in other languages are cognates: niwmonia in Welsh, niumoan in Manx, pneumonie in French, lunginflammation in Swedish, and so forth.

Description Many diseases and chemical exposures can cause pneumonia (Table 3.5), which means inflammation of the lungs with consolidation—a condition in which some of the alveolar lung Table 3.5 Forms of Pneumonia Name


Bacterial Acinetobacter pneumonia Actinomycosis Branhamellosis Chlamydial pneumonia Chronic pneumonia E. coli pneumonia Friedlander’s pneumonia Haemophilus (Hib) pneumonia Inhalation anthrax Legionellosis Melioidosis Meningococcal pneumonia Mycoplasmal pneumonia Pasteurellosis Pertussis pneumonia Pneumococcal pneumonia Pneumonic plague Psittacosis Pulmonary nocardiosis Q fever (may lead to BOOP) Serratia pneumonia Staphylococcal pneumonia Tularemic pneumonia Typhoid pneumonia Walking pneumonia

Acinetobacter baumannii Actinomyces israelii, others Moraxella (Branhamella) catarrhalis Chlamydia trachomatis or C. pneumoniae Pseudomonas aeruginosa, others Escherichia coli Klebsiella pneumoniae Haemophilus influenzae Bacillus anthracis Legionella pneumophila, others Pseudomonas pseudomallei Neisseria meningitides, others Mycoplasma pneumoniae Pasteurella multocida Bordetella pertussis Streptococcus pneumoniae Yersinia pestis Chlamydia psittaci Nocardia asteroides, others Coxiella burnetii Serratia marcescens Staphylococcus aureus (including MRSA) Francisella tularensis Salmonella typhi Any mild pneumonia, often Mycoplasma

Viral Adenovirus pneumonia Cytomegalovirus pneumonia Epstein-Barr virus pneumonia

Adenovirus 7, others Human herpesvirus 5 Epstein-Barr virus (Continued)



Table 3.5 (Continued) Name


Giant cell pneumonia Hantavirus pulmonary syndrome Herpes pneumonia hMPV pneumonia Influenza pneumonia Measles pneumonia Parainfluenza pneumonia RSV pneumonia Severe acute respiratory syndrome Varicella pneumonia

Measles (rubeola) morbillivirus Sin Nombre virus, others Human herpesvirus 1 or others Human metapneumovirus Influenza A, B viruses Measles (rubeola) morbillivirus Parainfluenza viruses Respiratory syncytial virus SARS coronavirus Human herpesvirus 3

Fungal Aspergillosis Blastomycosis Coccidioidomycosis Cryptococcosis Histoplasmosis Moniliasis (candidiasis) Mucormycosis Paracoccidiomycosis Penicilliosis Pneumocystosis (may lead to BOOP) Sporotrichosis

Aspergillus flavus, A. fumigatus Blastomyces dermatitidis Coccidioides immitis Cryptococcus neoformans Histoplasma capsulatum Candida albicans, others Fungi of family Mucoraceae Paracoccidioides brasiliensis Penicillium marneffei Pneumocystis carinii, others Sporothrix schenckii

Parasitic Ancylostomiasis Ascariasis Paragonimiasis Pulmonary echinococcosis Pulmonary schistosomiasis Strongyloidiasis Toxoplasmosis

Ancylostoma duodenale, Necator americanus Ascaris lumbricoides Paragonimus westermani Echinococcus granulosis, E. multilocularis Schistosoma, several species Strongyloides stercoralis Toxoplasma gondii

Noninfectious Acute eosinophilic pneumonia Aspiration pneumonia Chemical pneumonia Desquamative pneumonia Epler’s pneumonia Exogenous lipoid pneumonia Extrinsic pneumonia

Cause unknown; drugs or allergens? Inhalation of food, drink, or vomit Inhalation of irritants or toxins Cause unknown Cause unknown; autoimmune? Aspiration of oil Allergic reaction

spaces are filled with blood cells and fibrin. Typical symptoms include a cough, fever, chest pain, and breathing difficulty. About 40 percent of all human cases of pneumonia result from infection with the bacterium Streptococcus pneumoniae (Figure 3.12). Many other cases follow viral diseases such as influenza. Several highly publicized disease outbreaks in recent decades were specific forms of pneumonia, although the media did not call them by that name. Examples include



Figure 3.12 Transmission electron micrograph of Streptococcus pneumoniae, the most common cause of pneumonia in humans. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

Legionnaires’ disease or legionellosis in 1976, hantavirus pulmonary syndrome in 1993, and SARS in 2003. The 1918 influenza pandemic may have owed its high death toll to secondary bacterial pneumonia.

Who Is at Risk? Children, elderly people, and those with compromised immune systems are at highest risk for severe pneumonia. Unusual forms of pneumonia often turn up in people with AIDS and organ transplant recipients taking immunosuppressant drugs. An example is Pneumocystis carinii (PC) pneumonia, one of the infections that doctors recognize as a “red flag” for possible AIDS or other conditions affecting the immune system (Case Study 3-11). People who work with livestock may also be at risk for some forms of pneumonia (Case Study 3-12).

The Numbers An estimated 4.3 million people die from pneumonia every year, including more than 60,000 in the United States. In 2008, WHO reported that pneumonia kills more children every year than AIDS, malaria, and measles combined. Even “rare” forms of pneumonia are not really rare; for example, some 25,000 U.S. residents contract legionellosis every year, and about 1,000 of them die.



History Case Study 3-11: Déjà Vu When AIDS made its debut in 1981 and its victims began to die from Pneumocystis pneumonia, few people realized that something similar had happened at least once before—an epidemic of this same atypical pneumonia, possibly associated with a retroviral disease and acquired T-cell deficiency. According to a 2005 article, Europe had such an epidemic between 1920 and 1963. It resembled AIDS, except that most victims were premature infants. The authors of the study hypothesized that the infectious agent might be a retrovirus that originated in West Africa and arrived in Germany in the 1920s with returning colonists. Likely routes of spread were similar to those later observed for HIV: sexual contact between adult carriers (who did not become ill), blood transfusions and other hospital procedures in wartime Europe, human donor milk, and placental transmission. For unknown reasons, this tragic epidemic peaked in the 1950s and then ended. Carleton Gajdusek proposed a similar explanation in 1976, the same year he received the Nobel Prize for his work on prions.

Case Study 3-12: Splat! In 2003 a pregnant ewe gave birth to twin lambs at an outdoor farmer’s market in Germany. After the ewe ate the placenta, the market staff covered the parturient fluids with straw but did not otherwise clean the area. Several hundred visitors stood near the pen and apparently inhaled contaminated aerosols. As it turned out, many of the sheep at the exhibit were infected with a bacterium called Coxiella burnetii, and nearly 300 people contracted Q fever—an atypical pneumonia also known as Balkan grippe, abattoir fever, coxiellosis, or Nine Mile agent. This was not the largest such outbreak; in Germany in 1954, more than 500 human cases were traced to an infected cow that aborted at a farmer’s market.

By the time Hippocrates (460–375 B.C.) became the father of modern medicine, pneumonia was an old story. The ancient Egyptians did a lot of digging and rock quarry work when they built the pyramids, and many developed silicosis (lung disease from dust inhalation), which is often associated with pneumonia. Egyptian papyri also refer to “remedies to drive out cough” and “putrefaction of mucus.” But even walking upright, living in caves, and building fires can adversely affect the lungs, and a full history of pneumonia would be a history of humankind.

Prevention and Treatment Proper nutrition, including adequate vitamin D, may help prevent pneumonia and other diseases. To avoid hantavirus pulmonary syndrome, wear a dust mask when sweeping areas that may contain rodent droppings. Water heaters should be set at a high enough temperature to inhibit the bacteria that cause legionellosis (without scalding people or wasting energy). The film of crud that builds up on shower curtains may contain bacteria that cause pneumonia, so it’s a good idea to clean or replace them. The pneumococcus (Streptococcus pneumoniae) vaccine protects babies against seven strains of this bacterium. Since the introduction of this vaccine in 2000, rates of infection with these strains have declined by 85 percent, but the other strains have become more common. Another vaccine protects against Haemophilus influenzae B (Hib), which also causes pneumonia. Influenza may lead to pneumonia, so annual flu shots are a good idea.

Popular Culture Everyone has heard that we can “catch pneumonia” by getting chilled, but the truth is more complicated. When cold weather drives people indoors, they are more likely to share respiratory diseases. Also, people feel chills when



ambient temperatures are low, but also when a fever is starting. Cold, dry air can cause a runny nose that might be mistaken for a respiratory infection. According to an old joke, the best way to cure a cold is to get wet and stand in front of an open window until the cold becomes pneumonia, which doctors know how to treat. But becoming chilled doesn’t cause pneumonia, and doctors can’t always cure pneumonia anyway. A 2007 study concluded that overweight people are less likely than others to die from pneumonia. Popular discourse translated this finding to mean that obesity confers resistance. In fact, the same study found that obese people are more likely than others to die from diabetes or kidney disease, so they might simply die of something else before pneumonia gets them. American and European folk remedies for pneumonia include snakeroot (Aristolochia serpentaria and others) goldenseal (Hydrastis canadensis), peach, elderflower tea, catnip, deer blood mixed with wine, the feces of a white dog, or a poultice containing any of the following: mustard and flaxseed, potato, cabbage, hops, lobelia, onion, cornmeal mixed with onion, or mashed garlic. Other dubious cures include inhaling nettle fumes in a sweat lodge or placing a boiled onion in each armpit. Traditional Chinese herbal remedies for bacterial pneumonia include concoctions of reed (Phragmites communis), Job’s-tears (Coix lacryma-jobi), honeysuckle (Lonicera sp), dandelion (Taraxacum officinale), almond (Prunus dulcis), and ma huang (Ephedra sinica), plus inorganic ingredients such as gypsum powder.

The Future Air pollution is increasing in many parts of the world, and irritated or damaged lungs are susceptible to infection. The economic recession of 2009 may be another risk factor; unemployed people sometimes turn off their air conditioners during summer smog alerts, burn wood to keep warm in winter, avoid seeing doctors, or accept “dirty” jobs with employers who try to cut corners by not providing adequate personal protective equipment. Malnourished children are also susceptible to pneumonia.

References and Recommended Reading Bartram, J., et al. (Eds.) “Legionella and the Prevention of Legionellosis.” World Health Organization, 2007. Brooks, W. A., et al. “Human Metapneumovirus Infection among Children, Bangladesh.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1611–1613. Cunha, B. A. “The Atypical Pneumonias: Clinical Diagnosis and Importance.” Clinical Microbiology and Infection, Vol. 12 (Suppl 3), 2006, pp. 12–24. Fulhorst C. F., et al. “Hantavirus and Arenavirus Antibodies in Persons with Occupational Rodent Exposure.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 532–538. Goldman, A. S., et al. “What Caused the Epidemic of Pneumocystis Pneumonia in European Premature Infants in the Mid-20th Century?” Pediatrics, 2 May 2005. Greenwood, B. “A Global Action Plan for the Prevention and Control of Pneumonia.” Bulletin of the World Health Organization, Vol. 86, 2008, pp. 322–323. Hatfield, G. 2004. Encyclopedia of Folk Medicine. Santa Barbara, CA: ABC-CLIO. Hay, D. “Beware of Legionella Bacteria.” Seattle Times, 3 May 2008. Heikkinen, T., et al. “Human Metapneumovirus Infections in Children.” Emerging Infectious Diseases, Vol. 14, 2008, pp. 101–106. Hsieh, Y. C., et al. “The Transforming Streptococcus pneumoniae in the 21st Century.” Chang Gung Medical Journal, Vol. 31, 2008, pp. 117–124.



Huss, A., et al. “Efficacy of Pneumococcal Vaccination in Adults: a Meta-Analysis.” Canadian Medical Association Journal, Vol. 180, 2009, pp. 48–58. Jonsson, C. B., et al. “Treatment of Hantavirus Pulmonary Syndrome.” Antiviral Research, Vol. 78, 2008, pp. 162–169. Kelt, D. A., et al. “Threat of Hantavirus Pulmonary Syndrome to Field Biologists Working with Small Mammals.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1285–1287. Klugman, K. P. “Time from Illness Onset to Death, 1918 Influenza and Pneumococcal Pneumonia.” Emerging Infectious Diseases, Vol. 15, 2009, pp. 346–347. Levine, J. R., et al. “Occupational Risk of Exposure to Rodent-Borne Hantavirus at US Forest Service Facilities in California.” American Journal of Tropical Medicine and Hygiene, Vol. 78, 2008, pp. 352–357. Mangiarotti, P., and E. Pozzi. “Emergence of New Pneumonia: Besides Severe Acute Respiratory Syndrome.” Minerva Medica, Vol. 97, 2006, pp. 395–409. [Italian] McQuiston, J. H., et al. “Q Fever.” Journal of the American Veterinary Medical Association, 15 September 2002. “Pneumonia Kills More Children than AIDS, Malaria and Measles.” Press Trust of India Ltd., 3 May 2008. Porten, K., et al. “A Super-Spreading Ewe Infects Hundreds with Q Fever at a Farmer’s Market in Germany.” BMC Infectious Diseases, 6 October 2006. Roth, D. E., et al. “Acute Lower Respiratory Infections in Childhood: Opportunities for Reducing the Global Burden through Nutritional Interventions.” Bulletin of the World Health Organization, Vol. 86, 2008, pp. 356–364. Rubinstein, E., et al. “Pneumonia Caused by Methicillin-Resistant Staphylococcus aureus.” Clinical Infectious Diseases, Vol. 46 (Suppl 5), 2008, pp. S378–S385. Rudan, I., et al. “Epidemiology and Etiology of Childhood Pneumonia.” Bulletin of the World Health Organization, Vol. 86, 2008, pp. 408–416. Scott, J. A. G., et al. “Pneumonia Research to Reduce Childhood Mortality in the Developing World.” Journal of Clinical Investigation, Vol. 118, 2008, pp. 1291–1300. Straus, W. L., et al. “Risk Factors for Domestic Acquisition of Legionnaires Disease.” Archives of Internal Medicine, Vol. 156, 1996, pp. 1685–1692. Zeier, M., et al. “New Ecological Aspects of Hantavirus Infection: A Change of a Paradigm and a Challenge of Prevention—a Review.” Virus Genes, Vol. 30, 2005, pp. 157–180. Zuger, A. “‘You’ll Catch Your Death!’ An Old Wives’ Tale? Well . . .” New York Times, 4 March 2003.

WHAT ABOUT MENINGITIS AND ENCEPHALITIS? Summary of Threat Meningitis and encephalitis are dangerous, but neither one is a single disease. Meningitis is inflammation of the membranes that cover the brain and spinal cord, and encephalitis is inflammation of the brain itself. Many diseases, including most of the examples in Chapters 2 and 3, can lead to meningitis or encephalitis as a complication. Many other diseases can cause primary meningitis or encephalitis. Other Names Believe it or not, spinal meningitis was once called Simple Smiling Jesus—either because the two phrases have a vaguely similar cadence, or because meningitis victims supposedly grimace and bear their burdens gracefully (particularly if they are in a coma). Names such as spinal meningitis or cerebral meningitis refer to the part of the central nervous system affected. Aseptic meningitis is caused by a virus rather than a bacterium. Bacterial



meningitis was once called spotted fever or purples because of the rash. Names in other languages are mostly cognates, such as méningite (French), menenjit (Turkish), and meningjit (Albanian). The Czech term for meningitis, zánˇet mozkovy´ch blan, means literally “cerebral membrane inflammation.” Names for encephalitis include cephalitis, phrenitis, brain fever, swelling of the brain, dropsy of the brain, sleeping sickness, and swamp sickness. Historians describe the form that caused the great epidemic of 1915–1926 (and others) as encephalitis lethargica, von Economo’s syndrome, Economo-Cruchet disease, or Redlich’s syndrome. Names for encephalitis in other languages include encefalitis (Spanish), ansefalit (Turkish), and enkefaliitti (Finnish). The Indonesian term, penyakit otak, means “brain disease.”

Description Like pneumonia, these two terms—meningitis and encephalitis—refer to processes and symptoms rather than specific diseases. As stated earlier, meningitis is inflammation of the membranes that cover the brain and spinal cord, and encephalitis is inflammation of the brain itself. As a general (but not absolute) rule, most serious cases of meningitis are bacterial, and most serious cases of encephalitis are viral. In the United States, the best-known examples are meningococcal meningitis and West Nile encephalitis. Toxic chemicals, injuries, and autoimmune disease can also cause meningitis or encephalitis (Tables 3.6 and 3.7). Bacterial meningitis usually starts with a high fever, stiff neck, headache, confusion, nausea, and a rash. Even with treatment, many cases result in deafness, blindness, mental retardation, seizures, or even shock and death within as little as 24 hours. Political activist Helen Keller (1880–1968) became blind and deaf as a result of childhood meningitis. Yet most people who carry the meningococcus in their nasal passages do not become sick. Encephalitis often begins with similar symptoms—fever, neck pain, headache, drowsiness, and nausea. Severe cases may cause convulsions, coma, or paralysis. Some forms of encephalitis,

Table 3.6 Forms of Meningitis Name Bacterial Actinomycosis meningitis Anthrax meningitis Bacteroides meningitis Bartonellosis meningitis Campylobacter meningitis Dog bite fever Enterobacter meningitis GBS Meningitis Gonococcal meningitis Hib meningitis Klebsiella meningitis Legionella meningitis Listerial meningitis Lyme neuroborreliosis

Agent Actinomyces israeli and related species Bacillus anthracis Bacteroides species Bartonella henselae Campylobacter jejuni and related species Capnocytophaga canimorsus Enterobacter sakazakii Group B Streptococcus Neisseria gonorrhoeae Haemophilus influenzae serotype B Klebsiella pneumoniae Legionella pneumophila, others Listeria monocytogenes Borrelia burgdorferi (Continued)

Table 3.6 (Continued) Name


Melioidosis Meningococcal meningitis Mycoplasma meningitis Neonatal meningoencephalitis Pseudomonas meningitis Pneumococcal meningitis Rhodococcus meningitis Salmonella meningitis Serratia meningitis Staphylococcal meningitis Streptococcal meningitis Syphilitic meningitis Tuberculous meningitis Typhoid meningitis Yersiniosis

Pseudomonas pseudomallei Neisseria meningitides Mycoplasma pneumoniae Bacillus cereus, others Pseudomonas aeruginosa Streptococcus pneumoniae Rhodococcus equi Salmonella typhi or related species Serratia marcescens Staphylococcus epidermidis Streptococcus pneumoniae, S. suis, others Treponema pallidum Mycobacterium tuberculosis Salmonella typhi Yersinia enterocolitica

Viral Adenovirus meningitis California meningitis Colorado tick fever meningitis Congenital rubella meningitis Coxsackievirus meningitis Eastern equine meningitis Echovirus meningitis Enterovirus meningitis Hendra virus meningitis Herpes meningitis La Crosse meningitis Lymphocytic choriomeningitis Measles meningitis Mumps meningitis Poliovirus meningitis Rabies meningoencephalitis St. Louis meningitis TOSV meningitis Western equine meningitis

Adenovirus California virus (same as La Crosse) Colorado tick fever virus Rubella virus Coxsackievirus B, others Eastern equine encephalitis virus Echovirus 13, others Enterovirus 71, others Hendra virus HHV-1, -2, -3, -4, -5, -6 La Crosse virus Lymphocytic choriomeningitis virus Measles (rubeola) morbillivirus Mumps virus Poliovirus Rabies virus St. Louis encephalitis virus Toscana virus Western equine encephalitis virus

Fungal Aspergillosis Blastomycotic meningitis Cryptococcal meningitis Histoplasmosis meningitis Scedosporiosis Systemic candidiasis Torulopsis meningitis

Aspergillus fumigatus and related species Blastomyces dermatitidis Cryptococcus neoformans Histoplasma capsulatum Scedosporium apiospermum Candida albicans and related species Torulopsis glabrata

Parasitic African trypanosomiasis Chagas disease Human myiasis Primary amebic meningoencephalitis

Trypanosoma brucei Trypanosoma cruzi Fly larvae, various species Naegleria fowleri, Balamuthia mandrillaris

Noninfectious Biotinidase deficiency Complement receptor deficiency Hemophagocytic reticulosis Traumatic meningitis Vogt-Koyanagi-Harada syndrome

Genetic Genetic Genetic Head injury Cause unknown, possibly infectious

Note: Many pathogens can cause both meningitis and encephalitis (see Table 3.7).

Table 3.7 Forms of Encephalitis Name


Bacterial Actinomycosis encephalitis Bacteroides encephalitis Bartonellosis encephalitis Campylobacter encephalitis Dog bite fever E. coli encephalitis Enterobacter encephalitis GBS encephalitis Hib encephalitis Human monocytic ehrlichiosis Klebsiella encephalitis Listeriosis encephalitis Lyme encephalitis Meningococcal encephalitis Mycobacterial encephalitis Neonatal meningoencephalitis Pneumococcal encephalitis Pontiac fever encephalitis Pseudomonas encephalitis Staphylococcal encephalitis Streptococcal encephalitis Syphilis (secondary or congenital) Typhoid encephalitis Yersiniosis

Actinomyces israeli and related species Bacteroides species Bartonella henselae Campylobacter jejuni and related species Capnocytophaga canimorsus Escherichia coli Enterobacter sakazakii Group B Streptococcus Haemophilus influenzae serotype B Ehrlichia chaffeensis Klebsiella pneumoniae Listeria monocytogenes Borrelia burgdorferi Neisseria meningitides Mycobacterium avium or M. intracellulare Bacillus cereus, others Streptococcus pneumoniae Legionella pneumophila Pseudomonas aeruginosa Staphylococcus aureus Streptococcus pneumoniae, S. suis, others Treponema pallidum Salmonella typhi Yersinia enterocolitica

Viral Adenovirus encephalitis Bosin’s disease California encephalitis Central European tick-borne encephalitis Chandipura virus encephalitis Colorado tick fever encephalitis Cytomegalovirus encephalitis Dawson’s encephalitis Dengue encephalitis Eastern equine encephalitis Echovirus encephalitis Enterovirus encephalitis

Adenovirus Measles (rubeola) morbillivirus California virus (same as La Crosse) TBE virus Chandipura virus Colorado tick fever virus Cytomegalovirus (HHV-5) Measles (rubeola) morbillivirus Dengue 2 and 3 viruses Eastern equine encephalitis virus Echovirus Type 9 and others Enterovirus 71, others (Continued)



Table 3.7 (Continued) Name


Hendra virus encephalitis Hepatitis C encephalomyelitis Herpes encephalitis HIV encephalitis Human Vilyuisk encephalitis Influenza encephalitis Japanese encephalitis Kumlinge virus encephalitis La Crosse encephalitis Louping Ill encephalitis Lymphocytic choriomeningitis Measles encephalitis Mumps encephalitis Murray Valley encephalitis Nipah virus encephalitis Poliovirus encephalitis Powassan encephalitis Progressive rubella panencephalitis Rabies encephalitis St. Louis encephalitis Van Bogaert encephalitis Varicella-zoster encephalitis Venezuelan equine encephalitis West Nile encephalitis Western Equine encephalitis

Hendra virus Hepatitis C virus HHV-1, -2, -3, -4, -5, or -6 HIV-1 Vilyuisk human encephalitis virus Influenza A and B viruses Japanese encephalitis Kumlinge virus La Crosse virus Louping Ill virus Lymphocytic choriomeningitis virus Measles (rubeola) morbillivirus Mumps virus Murray Valley encephalitis virus Nipah virus Poliovirus Powassan virus Rubella virus Rabies virus St. Louis encephalitis virus Measles (rubeola) morbillivirus Varicella-zoster virus (HHV-3) Venezuelan equine encephalitis virus West Nile virus Western Equine encephalitis virus

Fungal Aspergillosis Blastomycotic encephalitis Chaetomium encephalitis Cryptococcal encephalitis Histoplasmosis Systemic candidiasis Valley fever

Aspergillus fumigatus and related species Blastomyces dermatitidis Chaetomium atrobrunneum Cryptococcus neoformans Histoplasma capsulatum Candida albicans and related species Coccidioides immitis

Parasitic Amebic encephalitis Amebic encephalitis Angiostrongyliasis Granulomatous amebic encephalitis Malarial encephalitis Schistosomiasis Toxoplasmosis Trypanosomiasis

Balamuthia mandrillaris Sappinia diploidea Angiostrongylus cantonensis Acanthamoeba keratitis Plasmodium falciparum and related species Schistosoma japonicum Toxoplasma gondii Trypanosoma brucei, T. cruzi

Noninfectious Acute disseminated encephalitis Behçet’s disease Cholesteatoma Familial histiocytic reticulosis Hashimoto’s encephalitis

Autoimmune disease Autoimmune disease Genetic or after injury Genetic Autoimmune disease?


Kawasaki disease Rasmussen encephalitis Systemic lupus erythematosus Traumatic encephalitis


Cause unknown, possibly infectious Autoimmune disease? Autoimmune disease After head injury

Note: Many pathogens can cause both encephalitis and meningitis (see Table 3.6).

such as rabies and Nipah (Figure 3.13), have a very high death rate. In the United States, the most dangerous viral mosquito-borne encephalitis is probably eastern equine, but there are only about five reported cases each year. In 2007, a visiting Scotsman caught eastern equine encephalitis and fell into a coma, but eventually recovered.

Who Is at Risk? Everyone is susceptible, but young people in crowded situations are at higher risk for bacterial meningitis, whereas older adults and those exposed to mosquito bites are prime candidates for viral encephalitis. AIDS is also a risk factor, both because the immune system is suppressed and because HIV itself can cause encephalitis. Since measles, mumps, and other diseases can cause encephalitis or meningitis, unvaccinated people are also at risk. For unknown reasons, African Americans are more likely than Caucasians to contract meningitis, but less likely to become deaf as a result. Having epidural anesthesia, handling live bats, drinking unpasteurized milk, eating inadequately cooked garden slugs, sharing tattoo needles, playing beer pong, swimming in a warm lake without a nose clip, and aspirating polluted water are risk factors for specific (and mostly rare) forms of meningitis or encephalitis.

The Numbers Meningococcal meningitis often affects college students, military recruits, or other healthy young adults (see Case Study 3-13). There are about 3,000 reported cases every year in the United States (including 100 to 125 on college campuses) and 500 cases per year in New Zealand. The largest recorded outbreak was in western Africa in 1996, with 250,000 reported cases and 25,000 deaths. In most outbreaks, the mortality rate ranges from 4 percent to 40 percent, and 11 to 19 percent of survivors have longterm deficits. The estimated annual incidence of acute encephalitis is 6 per 100,000 population worldwide. In 2005, Japanese encephalitis killed more than 1,100 people in northern India and Nepal, most of them children. (There is an effective vaccine, but it was not available to most people at the time.)

Case Study 3-13: Going Forth At least once a year, the press terrifies American families by highlighting a college student’s tragic death from meningococcal meningitis. Within 24 hours after contracting this disease, often in a crowded setting such as a college dormitory, a previously healthy young adult is dead. And the debate starts over: Maybe I shouldn’t live in a dorm? Look what happened to that other guy. But I can’t afford my own apartment. Maybe I should get a shot? But they say it doesn’t work half the time. Besides, the shot might make me sick, and midterms are next week. And Mom lost her insurance, and the shot costs $120. Would I rather have a chemistry textbook or a meningitis shot? Let’s wait and see if anybody else on campus gets sick.



Figure 3.13 Transmission electron micrograph showing Nipah virus, the agent of an emerging disease in humans. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



In 1998–1999, Nipah encephalitis infected 265 people in Malaysia and killed 105. The death rate was 40 percent, and many survivors had permanent brain damage. Nipah also infected horses, cats, dogs, goats, and pigs. Public health authorities reportedly ended the outbreak by slaughtering nearly 1 million pigs. In 2005, a food-borne Nipah outbreak killed 11 of 12 infected people (92 percent).

History The Austrian scientist Anton Weichselbaum (1845–1920) discovered the agent of meningococcal meningitis in 1887, and the American physician Simon Flexner (1863–1946) was the first to treat it successfully using an antiserum obtained from horses. The prognosis improved with the discovery of sulfa drugs in the 1930s and penicillin in the 1940s, but mortality remains at about 10 percent. In the 1990s, Disney World in Florida had to close earlier in the evening than usual due to repeated outbreaks of St. Louis encephalitis (which is spread by mosquitoes that are active after dark). In 1990, Florida had 184 cases and seven deaths. The problem might have resulted from the reduction of vector control programs.

Prevention and Treatment The most common causes of encephalitis are probably the herpes simplex virus, which is hard to avoid, and the varicella-zoster virus, which lurks in most people who have had chickenpox. Bacterial meningitis is also hard to avoid, because people usually catch it by contact with one another. An element of luck is also involved; for every young adult who contracts fatal meningitis, thousands of others are infected without ever having symptoms. As of 2009, the most widely used meningococcus vaccine protects against only four of the seven most common Neisseria meningitidis serogroups (A, C, Y, and W-135). This vaccine does not prevent infection with serogroup B, Case Study 3-14: Waking Up which causes nearly half of all cases in the Between 1915 and 1930, a mysterious panUnited States and more than half of all fatal demic known popularly as “sleepy sickcases in Sweden. The vaccine is still better than ness” caused thousands of people to lapse nothing. In 2009, human vaccines are also availinto a semiconscious state with a masklike able for Japanese encephalitis and Venezuelan facial appearance. About 20 to 40 percent equine encephalitis, but not for St. Louis, La of these patients died; some recovered, but later developed neurological problems; Crosse, eastern equine, western equine, or West others simply remained semiconscious, in Nile encephalitis.

Popular Culture Oliver Sacks’ 1973 book Awakenings, and the 1990 motion picture, explore the lives of real people who woke from a semi-comatose state some fifty years after contracting encephalitis lethargica in the 1915–1930 epidemic (Case Study 3-14).

some cases for decades, until doctors awakened them (temporarily) with drugs used to treat Parkinson’s disease. Similar outbreaks occurred in Italy in 1889–1890 and in Iceland in 1948–1949. The agent was never identified, and some sources claim it no longer exists, but sporadic cases continue to turn up, sometimes after a disease such as herpes zoster, bartonellosis, or a Streptococcus infection.



North American and European folk remedies for “brain fever” (encephalitis) include ginger and boneset tea. Chinese herbal remedies for meningitis include shepherd’s-purse (Capsella bursa-pastoris), Japanese holly fern (Cyrtomium fortunei), mulberry leaves (Morus sp.), weeping forsythia (Forsythia suspensa), mint, licorice, almonds, honeysuckle flowers (Lonicera sp.), or bamboo shoots; or, if high fever is present, a concoction of rhinoceros or buffalo horn with figwort, sage, Chinese peony, and other herbs. For mosquito-borne encephalitis, treatments include purple giant hyssop (Agastache rugosa), Persian shield (Strobilanthes sp.), gardenia (Gardenia florida), aster (Aster trinervius), or border grass (Liriope sp.). Rhinoceros or buffalo horn was added to the mix in severe cases.

The Future In 2007, pharmaceutical companies in the United Kingdom and India announced progress in developing a vaccine that would protect against all five serogroups of meningococcal meningitis. As of 2009, no such vaccine is yet available. The world also needs a meningococcal vaccine for infants and toddlers and a human vaccine for West Nile.

References and Recommended Reading Bulakbasi, N., and M. Kocaoglu. “Central Nervous System Infections of Herpesvirus Family.” Neuroimaging Clinics of North America, Vol. 18, 2008, pp. 53–84. Byrd, T. F., and L. E. Davis. “Multidrug-Resistant Tuberculous Meningitis.” Current Neurology and Neuroscience Reports, Vol. 7, 2007, pp. 470–475. Chua, K. B., et al. “Nipah Virus: A Recently Emergent Deadly Paramyxovirus.” Science, Vol. 288, 2000, pp. 1432–1435. Czermak, M., and T. Jean. “Von Economo-Cruchet Lethargic Encephalitis and its Relation to HIV Infection.” L’Encéphale, Vol. 16, 1990, pp. 375–82. [French.] Dourmashkin, R. R. “What Caused the 1918–30 Epidemic of Encephalitis Lethargica?” Journal of the Royal Society of Medicine, Vol. 90, 1997, pp. 515–520. Ewald, A. J., and D. B. McKeag. “Meningitis in the Athlete.” Current Sports Medicine Reports, Vol. 7, 2008, pp. 22–27. Fitch, M. T., et al. “Emergency Department Management of Meningitis and Encephalitis.” Infectious Disease Clinics of North America, Vol. 22, 2008, pp. 33–52. Garrett, L. A. “Complacency Boosts West Nile Peril.” Los Angeles Times, 6 September 2004. Gould, E. A., and T. Solomon. “Pathogenic Flaviviruses.” Lancet, Vol. 371, 2008, pp. 500–509. Gurley, E. S., et al. “Person-to-Person Transmission of Nipah Virus in a Bangladeshi Community.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1031–1037. Halperin, J. J. “Nervous System Lyme Disease.” Infectious Disease Clinics of North America, Vol. 22, 2008, pp. 261–274. Hviid, A., et al. “Mumps.” Lancet, Vol. 371, 2008, pp. 932–944. Jmor, F., et al. “The Incidence of Acute Encephalitis Syndrome in Western Industrialized and Tropical Countries.” Virology Journal, October 2008. Katragkou, A., et al. “Scedosporium apiospermum Infection after Near-Drowning.” Mycoses, Vol. 50, 2007, pp. 412–421. Keynan, Y., and E. Rubinstein. “The Changing Face of Klebsiella pneumoniae Infections in the Community.” International Journal of Antimicrobial Agents, Vol. 30, 2007, pp. 385–389. Lo, M. K., and P. A. Rota. “The Emergence of Nipah Virus, a Highly Pathogenic Paramyxovirus.” Journal of Clinical Virology, Vol. 43, 2008, pp. 396–400. Luby, S. P., et al. “Foodborne Transmission of Nipah Virus, Bangladesh.” Emerging Infectious Diseases, Vol. 12, 2006, pp. 1888–1894.



McCall, S., et al. “The Relationship Between Encephalitis Lethargica and Influenza: A Critical Analysis.” Journal of Neurovirology, Vol. 14, 2008, pp. 177–185. Pace, D., and A. J. Pollard. “Meningococcal A, C, Y and W-135 Polysaccharide-Protein Conjugate Vaccines.” Archives of Disease in Childhood, Vol. 92, 2007, pp. 909–915. Salleh, A. “Man’s Brain Infected by Eating Slugs.” ABC Science Online, 20 October 2003. Schneider, J. I. “Rapid Infectious Killers.” Emergency Medicine Clinics of North America, Vol. 22, 2004, pp. 1099–1115. Schut, E. S., et al. “Community-Acquired Bacterial Meningitis in Adults.” Practical Neurology, Vol. 8, 2008, pp. 8–23. Seijvar, J. J. “The Long-Term Outcomes of Human West Nile Virus Infection.” Clinical Infectious Diseases, Vol. 44, 2007, pp. 1617–1624. Smith, T. C., et al. “Exposure to Streptococcus suis Among U.S. Swine Workers.” Emerging Infectious Diseases, Vol. 14, 2008, pp. 1925–1927. Stone, M. J., and C. P. Hawkins. “A Medical Overview of Encephalitis.” Neuropsychological Rehabilitation, Vol. 17, 2007, pp. 429–449. Teyssou, R., and E. Muros-Le Rouzic. “Meningitis Epidemics in Africa: A Brief Overview.” Vaccine, Vol. 25 (Suppl. 1), pp. A3–A7. Weingartl, H. M., et al. “Recombinant Nipah Virus Vaccines Protect Pigs Against Challenge.” Journal of Virology, Vol. 80, 2006, pp. 7929–7938. Woodard, J. L., and D. M. Berman. “Prevention of Meningococcal Disease.” Fetal and Pediatric Pathology, Vol. 25, 2006, pp. 311–319. Yu, H., et al. “Human Streptococcus suis Outbreak, Sichuan, China.” Emerging Infectious Diseases, Vol. 12, 2006, pp. 914–920.

CONCLUSION We aren’t quite finished yet. These ten direct biological threats, and thousands more, occupy an ever-changing world that largely determines the level of risk. So what sort of world do these threats share with us? What can humans do about indirect biological threats that destroy food and other key resources? And are there any global trends in progress that might increase or decrease the associated risk?

This page intentionally left blank


Food Insecurity

I am aware of some of the tragic repercussions of the chemical fight against insects taking place in France and elsewhere and I deplore them. Modern man no longer knows how to foresee and forestall. He will end by destroying the earth from which he and other living creatures draw their food. Poor bees, poor birds, poor men. —Albert Schweitzer, 1956 letter to a French beekeeper

“Food insecurity” is a modern euphemism for hunger or the reasonable expectation of hunger. As of 2009, it affects billions of people. Chapters 2 and 3 describe infectious diseases that directly threaten humans, but the story doesn’t end there. Hundreds of diseases and pests team up with weather and mismanagement every year to attack the human food supply (Table 4.1), more successfully in some regions than others. Starving people become highly vulnerable to infectious diseases, such as tuberculosis, malaria, and pneumonia. This chapter describes some biological threats to livestock species that represent an important component of the human food supply, including cattle, sheep, pigs, chickens—and bees.

WHAT ABOUT BEES? In recent years, the Internet has buzzed with a quotation attributed to Albert Einstein: “If the bee disappeared then man would have only four years to live. No more bees, no more pollination, no more plants, no more animals, no more men.” The statement is nonsense, and there is no evidence that Einstein said it; but the warning persists, often in conjunction with true reports of honeybee disease epidemics. The most likely source of this urban legend is a vaguely similar statement by Albert Schweitzer, not Einstein (quoted at the top of this page). Although written in 1956, this warning first reached a large audience at a Schweitzer symposium in 1992. By 1994, the quotation attributed to Einstein appeared in a pamphlet distributed by the National Union of French Apiculture. In other words, it appears that somebody got the names mixed up.



Table 4.1 Some Outbreaks of Animal Diseases Disease Anthrax Anthrax Anthrax Rinderpest Rinderpest Rinderpest Mad Cow/BSE Foot-and-mouth Heartwater Classical swine fever Blue-ear pig disease Newcastle disease Newcastle disease Avian influenza Varroa bee mite *

Year 1979–1980 2004 2006 1600s 1890s 1983 1986–1996 2001 1998 1997–1998 2007 1971–1974 1973 1983–1984 1985–1995


Loss or Cost

Zimbabwe Zimbabwe Saskatchewan Europe South Africa Nigeria England England Eastern Cape Netherlands China Southern California Northern Ireland Northeastern United States North America

Many cattle, 182 humans Thousands of wild mammals 804 farm animals 200 million cattle 90% of all cattle 1 million cattle 179,000 cattle* 4 million cattle 214 million Rand 11 million pigs 1 million pigs 12 million chickens 260,000 chickens 17 million chickens 95% of wild honeybees

Plus an estimated 4.4 million cattle slaughtered as a control measure, and 140+ human deaths from vCJD.

Neither Schweitzer nor Einstein mentioned a four-year time frame, but many sources state that the loss of all bees could reduce food production by 25 to 33 percent. Might someone have interpreted the lower number to mean that one-fourth of humanity (including one-fourth of the farmers) would starve every year, and in four years we would all be gone? This is the type of goofy reasoning that underlies many pseudoscientific claims. Besides ignoring the rules of exponential decay, the scenario overlooks obvious alternatives, such as planting more crops that are not dependent on bees, using artificial pollination, or simply sharing food. Most adults in developed nations could survive a 25 percent reduction in daily caloric intake. (In 2003, according to the United Nations Food and Agriculture Organization, the average American adult consumed 3,770 calories per day and needed about 2,200.) Even if mankind is not facing imminent extinction, however, many crops do need bees, and we will return to this topic. But since bees are seldom uppermost in the public consciousness, we will start with a scary disease that everyone has read about. MAD COW DISEASE Summary of Threat Bovine spongiform encephalopathy (BSE), or mad cow disease, is a poorly understood, fatal illness that apparently results from a change in the shape of certain proteins in the brain. Similar diseases occur in other mammals, including humans, and the infectious agents may cross species boundaries in food or blood products. BSE is classified as a biosecurity threat under the Bioterrorism Protection Act of 2002. Other Names Similar diseases in other mammals include scrapie in sheep and goats; chronic wasting disease (CWD) in deer, elk, and moose; transmissible mink encephalopathy (TME) in farmed mink;



feline spongiform encephalopathy (FSE) in cats; an unnamed prion disease in squirrels; and Creutzfeldt-Jakob disease (CJD) and kuru in humans. As a group, these diseases are called transmissible spongiform encephalopathies (TSE). When people contract a TSE from contaminated meat, the result is called new variant Creutzfeldt-Jakob disease (vCJD or nvCJD). Mad cow disease is la vaca loca (“crazy cow”) in Spanish, gekke-koeienziekte (“cow madness”) in Dutch, and maladie des vaches folles (“disease of crazy cows”) in French.

Description BSE usually begins with an unsteady, trembling cow that loses its appetite and generally seems out of sorts. The cow may lick its nose, grind its teeth, or stand around with its head down (Figure 4.1). Eventually, the animal must be euthanized. BSE and related diseases are associated with abnormal membrane proteins called prions, which appear to transmit disease by inducing normal proteins to fold incorrectly. As of 2009, this is the most widely accepted explanation, but some researchers have proposed that prions are not the whole story. One theory is that small bacteria called spiroplasma are the underlying cause. Others claim that pesticides, trace metals, or toxins in animal feed are contributing factors.

Figure 4.1 A “mad cow,” later found to have bovine spongiform encephalopathy. The animal showed abnormal posture, weight loss, and other symptoms of this disease. Source: USDA Animal and Plant Health Inspection Service (APHIS).



Which Animals Are at Risk? Case Study 4-1: Mad Squirrels Despite their popular image, wild squirrels and chipmunks often eat carrion or even kill live prey. As a result, they are exposed to the same biological threats as any other predator, including prion diseases. A 1997 paper in the journal Lancet described five patients who developed the neurological disease CJD after a history of eating squirrel brains, a culinary tradition in rural Kentucky. The authors of the paper reported that the brains are often scrambled with eggs or else cooked in a meat and vegetable dish known as burgoo.

Animals that eat infected meat or bone meal are the main risk group. Infected cows may also transmit the disease to their calves through the placenta. Studies suggest that a genetic mutation can increase the risk of BSE. If prions cause TSE, these diseases should appear only in species that eat meat or its byproducts (and those that undergo organ transplants or blood transfusions). Mink, cats, and humans are meat eaters, and until recently, mass-produced cattle and sheep were often fed recycled carrion. Wild squirrels also eat meat on a fairly regular basis (Case Study 4-1), and even wild deer have been observed munching on the carcasses of dead deer.

The Numbers As of 2009, about 300 people had died of variant Creutzfeldt-Jakob disease (Figure 4.2), including three in the United States. Most probably ate BSE-contaminated meat, but at least four contracted vCJD from transfusions. These numbers represent about 1 percent of the people who die of “normal” CJD during the same time period. At the height of the BSE epidemic in England, an estimated 179,000 cattle were infected, and 4.4 million were slaughtered to stop the epidemic. Since about 470,000 infected cattle had already entered the human food chain, no one can predict how many more human cases will appear.

History In 1997, Dr. Stanley B. Prusiner won a Nobel Prize for his discovery of prions. A generation earlier, in 1976, Dr. Daniel Carleton Gajdusek won a Nobel Prize for determining that an infectious agent similar to a slow virus caused both kuru and scrapie, but the exact nature of that agent was Prusiner’s contribution. On 19 September 1985, doctors in England examined Cow Number 133 (the first “mad cow”) and found the brain lesions now known as spongiform encephalopathy. The British government acknowledged the outbreak in 1986, and it peaked in 1992–1993. Yet there is evidence that a similar disease has existed since ancient times. The author’s 2002 book cites a nineteenthcentury account of abnormal behavior in Irish cows. In 2007, the journal New Scientist reported that the Roman writer Publius Flavius Vegetius Renatus described a similar cattle disease in the fifth century A.D. About ten years after the 1986 BSE outbreak, England suffered an outbreak of a similar neurological disease (CJD) in humans. First described in 1920, CJD was usually sporadic. Thus, the new disease was called variant or new variant CJD. The original source of the 1986 outbreak is unknown, but it might have been an infected antelope that died at a safari park and was made into meat and bone meal. Since about 1926, farmers had recycled animal remains into livestock food, but this practice was officially discontinued after scientists suspected a link to BSE. Feeding dead animals to cows might seem strange, but the rendering process usually kills bacteria or other pathogens. Prions are harder to kill, because they are not alive.



Figure 4.2 Light micrograph of human brain tissue showing amyloid plaques found in variant CreutzfeldtJakob disease, attributed to the prion that causes bovine spongiform encephalopathy (BSE) in cattle. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

Another theory is that cows caught the disease from humans. During the first half of the twentieth century, British cows allegedly ingested human remains that were imported from India as a component of animal feed.

Prevention and Treatment There is no known treatment for BSE in cattle or vCJD in humans. If future studies determine that TSE diseases require spiroplasma infection and do not result solely from prions, treatment with bactericidal agents may be an option. Meanwhile, the only known preventive measure is to avoid the use of mammalian proteins in farm animal food. Special decontamination procedures are necessary to ensure that surgical instruments are free of prions. In 2008, Canadian researchers reported a new urine test that may identify BSE biomarkers in living cattle. In 2007, a Japanese company announced the creation of genetically engineered cows with no prion proteins, normal or otherwise. This development is promising, but it is too recent to evaluate. Since prion proteins apparently occur in all unmodified mammals, one wonders if their absence might cause unexpected problems. Recent studies suggest that normal prion proteins may be involved in olfaction, memory, and other brain functions.



Popular Culture Prion diseases are perfect candidates for rumor and misconception. They are associated with hamburgers; they can make people go crazy and die; and they are as poorly understood today as bacterial and viral infections were a century ago. In the 2006 motion picture Mad Cowgirl, the chain-smoking, hard-drinking female protagonist— a slaughterhouse health inspector whose brother operates a meatpacking business—is so worried about contracting vCJD that she eats large quantities of rare beef, jumps in the sack with a series of disturbingly creepy men, fantasizes about extreme violence, and ends up losing her mind anyway. It turns out that she has a brain tumor, or perhaps a pseudotumor or a fantasy about a pseudotumor. One message is clear: people can destroy themselves without any help from exotic diseases. A 2004 book claims that Alzheimer’s disease is the result of a secret government study of kuru and BSE, as evidenced by decades of widely publicized cattle mutilations (which others have attributed to everything from space aliens to the legendary predator known as Chupacabra). The book claims that these mutilations are proof of an illegal sampling program. In fact, Alzheimer’s disease could be related to prions, but biologists who have examined the remains of allegedly mutilated cattle have come away singularly unimpressed. In the spring of 2008, South Korea decided to resume its imports of U.S. beef. In an effort to dispel public health fears of BSE after months of street protests, a group of South Korean doctors and business executives ate American sirloin steak at a highly publicized banquet. To our knowledge, none of them got sick. The Future Every time a mad cow turns up, the host nation’s beef is suspect, and the beef industry suffers. The beef byproducts industry is another victim, because meat-and-bone meal is no longer acceptable as animal feed. Since not even the biodiesel reaction can destroy its infectivity, this material is largely wasted. Worse, the inability of farmers to sell animal carcasses may encourage illegal disposal. Improved test methods may resolve this problem, and one of the alternative theories may even yield a cure.

References and Recommended Reading Altman, L.K. “U.S. Scientist Wins Nobel for Controversial Work.” New York Times, 7 October 1997. Belay, E. D., and L. B. Schonberger. “The Public Health Impact of Prion Diseases.” Annual Review of Public Health, Vol. 26, 2005, pp. 191–212. Berger, J. R., et al. “Creutzfeldt-Jakob Disease and Eating Squirrel Brains.” Lancet, Vol. 350, 1997, p. 642. Brown, D. “The ‘Recipe for Disaster’ that Killed 80 and Left a £5bn Bill.” The Telegraph, 19 June 2001. Broxmeyer, L. “Thinking the Unthinkable: Alzheimer’s, Creutzfeldt-Jakob and Mad Cow Disease: The AgeRelated Reemergence of Virulent, Foodborne, Bovine Tuberculosis or Losing Your Mind for the Sake of a Shake or Burger.” Medical Hypotheses, Vol. 64, 2005, pp. 699–705. Bruederle, C. E., et al. “Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production.” PLoS ONE, 13 August 2008. Callahan, J. R. “Squirrels as Predators.” Great Basin Naturalist, Vol. 53, 1993, pp. 137–144. Callahan, J. R. 2002. Biological Hazards: An Oryx Sourcebook. Westport, CT: Oryx Press (imprint of Greenwood Publishing Group). Colchester, A. C., and N. T. Colchester. “The Origin of Bovine Spongiform Encephalopathy: The Human Prion Disease Hypothesis.” Lancet, Vol. 366, 2005, pp. 856–861. Cosseddu, G. M., et al. “Advances in Scrapie Research.” Revue Scientifique et Technique, Vol. 26, 2007, pp. 657–668.



“Fourth Case of Transfusion-Associated vCJD Infection in the United Kingdom.” Eurosurveillance, 18 January 2007. Heaton, M. P., et al. “Prevalence of the Prion Protein Gene E211K Variant in US Cattle.” BMC Veterinary Research, Vol. 4, 2008, p. 25. Imrie, C. E., et al. “Spatial Correlation Between the Prevalence of Transmissible Spongiform Diseases and British Soil Geochemistry.” Environmental Geochemistry and Health, 22 April 2008. Lasmeras, C. J. “The Transmissible Spongiform Encephalopathies.” Revue Scientifique et Technique, Vol. 22, 2003, pp. 23–36. Lemmer, K., et al. “Decontamination of Surgical Instruments from Prions. II. In Vivo Findings with a Model System for Testing the Removal of Scrapie Infectivity from Steel Surfaces.” Journal of General Virology, Vol. 89, 2008, pp. 348–358. MacKenzie, D. “New Twist in Tale of BSE’s Beginnings.” New Scientist, 17 March 2007, p. 11. Marks, K. “Imported Antelope May Have Caused BSE Epidemic.” The Independent, 19 April 2001. Meikle, J. “Sudden Rise in BSE Alarms Scientists.” The Guardian, 24 November 2003. “New Mad-Cow Rule Poses Its Own Health Dangers.” Associated Press, 7 December 2008. “New Version of Mad Cow Suspected.” United Press International, 18 December 2008. Pennington, H. “Origin of Bovine Spongiform Encephalopathy.” Lancet, Vol. 367, 2006, pp. 297–298. Purdey, M. “The UK Epidemic of BSE: Slow Virus or Chronic Pesticide-Initiated Modification of the Prion Protein?” Medical Hypotheses, Vol. 46, 1996, pp. 445–454. Quaid, L. “U.S. Mad Cow Cases are Mysterious Strain.” Associated Press, 11 June 2006. Race, B. L., et al. “Levels of Abnormal Prion Protein in Deer and Elk with Chronic Wasting Disease.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 824–830. Richt, J. A., et al. “Production of Cattle Lacking Prion Protein.” Nature Biotechnology, Vol. 25, 2007, pp. 132–138. Richt, J. A., and S. M. Hall. “BSE Case Associated with Prion Protein Gene Mutation.” PLoS Pathogens, 12 September 2008. Simon, S. L., et al. “The Identification of Disease-Induced Biomarkers in the Urine of BSE Infected Cattle.” Proteome Science, Vol. 6, 2008, p. 23. Smith, P. G. “The Epidemics of Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Current Status and Future Prospects.” Bulletin of the World Health Organization, Vol. 81, 2003, pp. 123–130. Yokoyama, T., and S. Mohri. “Prion Diseases and Emerging Prion Diseases.” Current Medicinal Chemistry, Vol. 15, 2008, pp. 912–916.

FOOT-AND-MOUTH DISEASE Summary of Threat Foot-and-mouth disease (FMD) is a highly contagious viral disease of animals with cloven hoofs, including cattle, pigs, sheep, goats, and deer. It causes sores that interfere with feeding and movement. Although seldom fatal, it can spread rapidly through livestock populations and cause great economic losses. FMD is classified as a biosecurity threat under the Bioterrorism Protection Act of 2002. Other Names Foot-and-mouth disease is also called hoof-and-mouth disease, aphthous fever, aphtha disease, or aphthae epizooticae. Names in other languages include fiebre aftosa in Spanish, Maulund Klauenseuche in German, penyakit mulut dan kuku in Indonesian, and száj és körömfájás (“mouth and hoof ache”) in Hungarian. FMD is not related to a human disease called hand, foot,



Case Study 4-2: Phoenix the Calf At the height of England’s 2001 foot-andmouth disease crisis, Prime Minister Tony Blair made a gesture fraught with ancient symbolism and PR genius. Yielding to public demand or to a higher authority, he officially spared the life of Phoenix—a newborn white calf that somehow survived for five days under a heap of dead cattle, which farmers had recently slaughtered as part of the campaign to stop the epidemic. In the midst of disaster, there is nothing like a lone survivor to buoy the spirit (see also Case Study 4-7, Strong Pig).

and mouth disease or to an all-too-human behavioral tendency called “foot in mouth” (a lapse of diplomacy).


FMD causes fever and vesicles on the mouth, nipples, and feet (Figure 4.3), plus excessive salivation, lameness, and reluctance to move. The agent is one of the picornaviruses, a family that also includes the agents of polio and hepatitis A in humans. There are seven serotypes, each with many strains. As of 2009, FMD may be the most economically devastating livestock disease. At least 95 percent of infected cattle recover without treatment, but the disease spreads rapidly and reduces meat and milk production. Also, the World Organisation for Animal Health (OIE) does not allow a country to export animals unless it has been free of FMD without vaccination for at least a year. Thus, the usual way to stop an epidemic is to slaughter millions of animals (Case Study 4-2). Although many question this policy, it may be defensible on economic grounds.

Figure 4.3 Foot of a cow with foot-and-mouth disease, showing a ruptured vesicle in the cleft. Source: CSIRO Australian Animal Health Laboratory.



Which Animals Are at Risk? FMD spreads by contact, aerosol transmission, or ingestion of contaminated material. In a susceptible population, all animals show symptoms during an outbreak. The most highly publicized outbreaks have involved cattle, but the disease also affects pigs, sheep, goats, and many wildlife species, including deer and giraffes. Camels and hippopotami appear to be resistant. FMD is considered a zoonosis, and at least 50 human cases have occurred over the years. There are no reports of severe illness or transmission between humans.

The Numbers The 2001 epidemic in England resulted in the slaughter of 10 million animals at an estimated cost of $20 billion pounds sterling, but that was the tip of the iceberg. Associated losses per week during that epidemic included $12 million pounds to agriculture and $140 million pounds to the tourism industry.

History When German scientist Friedrich Loeffler discovered the FMD virus in 1897, farmers and veterinarians had already dealt with this disease for centuries. In 1834, three veterinarians in Germany each drank a quart of milk from an infected cow to test the hypothesis that humans could contract foot-and-mouth disease. It worked; all three developed symptoms. As of 2009, the most recent FMD outbreak in the United States was in 1914. Others occurred in England in 1967, 2001, and 2007, in Taiwan in 1997, and in China in 2005. In 1946, an FMD outbreak in Mexico threatened to spread north into Texas, and the U.S. and Mexican governments cooperated in a plan to destroy a large proportion of animals in affected areas. But rural Mexican farmers and ranchers responded with such violent protest that, within a year, both governments switched to the slower and more expensive strategy of vaccinating healthy livestock.

Prevention and Treatment The first FMD vaccines were ineffective and sometimes caused disease. A better vaccine— the world’s first genetically engineered vaccine—has been available since 1981, but it works only for a few months and only against similar strains. The cost of vaccinating all animals would be prohibitive, and vaccinated animals can be carriers. Countries with vaccination programs lose OIE “disease-free” status and can no longer export animals. Thus, until a better method is found, farmers rely on captive bolt guns and backhoes to control FMD epidemics. The key to controlling FMD is to keep it out.

Popular Culture In the 1963 motion picture Hud, the title character is the ruthless son of a wealthy Texas cattleman. When FMD infects the herd, Hud urges his father to sell the cattle quickly, before the



health inspectors find out. Hud’s question reflects an ongoing debate that continues to the present day: “You gonna let them shoot your cows out from under you on account of a schoolbook disease?” The law-abiding father prevails, and the cattle are slaughtered, in a scene that shocked 1963 audiences and critics. One conspiracy theory holds that FMD does not really exist, but was invented by evil government scientists as an excuse for slaughtering millions of cows and ruining farmers. It is not clear why any government would want to do this.

The Future Until recently, most FMD research in the United States took place at the Plum Island laboratory. In 2009, the Department of Homeland Security announced that a new facility in Manhattan, Kansas, will replace Plum Island starting in about 2014. A more effective and less expensive FMD vaccine, one that might make global eradication possible, is surely on every cattle rancher’s wish list.

References and Recommended Reading Alexandersen, S., and N. Mowat. “Foot-and-Mouth Disease: Host Range and Pathogenesis.” Current Topics in Microbiology and Immunology, Vol. 288, 2005, pp. 9–42. Bauer, K. “Foot-and-Mouth Disease as Zoonosis.” Archives of Virology Supplement, Vol. 13, 1997, pp. 95–97. Berríos, E. P. “Foot and Mouth Disease in Human Beings: a Human Case in Chile.” Revista Chilena de Infectología, Vol. 24, 2007, pp. 160–163. Brown, D., and A. McSmith. “Brown Scorns ‘Urban Legend of Cover-up.’” The Telegraph, 28 June 2001. “Contagious Cattle Disease Found in England.” United Press International, 4 August 2007. DeClerc, K., and N. Goris. “Extending the Foot-and-Mouth Disease Module to the Control of Other Diseases.” Developments in Biologicals, Vol. 119, 2004, pp. 333–340. “Foot and Mouth Disease Found in Kyrgyzstan.” United Press International, 27 February 2004. Grubman, M. J., and B. Baxt. “Foot-and-Mouth Disease.” Clinical Microbiology Reviews, Vol. 17, 2004, pp. 465–493. “Humans Test Negative for FMD in Britain, Animal Cases Continue to Decline.” Journal of the American Veterinary Medical Association, 1 June 2001. Kitching, P., et al. “Global FMD Control—Is It an Option?” Vaccine, Vol. 25, 2007, pp. 5660–5664. Kitching, R. P., et al. “Use and Abuse of Mathematical Models: An Illustration from the 2001 Foot and Mouth Disease Epidemic in the United Kingdom.” Revue Scientifique et Technique, Vol. 25, 2006, pp. 293–311. Lombard, M., et al. “A Brief History of Vaccines and Vaccination.” Revue Scientifique et Technique, Vol. 26, 2007, pp. 29–48. Mahy, B. W. “Introduction and History of Foot-and-Mouth Disease Virus.” Current Topics in Microbiology and Immunology, Vol. 288, 2005, pp. 1–8. Musser, J. M. 2004. “A Practitioner’s Primer on Foot-and-Mouth Disease.” Journal of the American Veterinary Medical Association, Vol. 224, 2004, pp. 1261–1268. Prempeh, H., et al. “Foot and Mouth Disease: The Human Consequences.” British Medical Journal, Vol. 322, 2001, pp. 565–566. Richardson, Z. “UC Davis Developing Model to Tackle Foot-and-Mouth Disease.” Food Chemical News, 15 January 2007. Rweyemamu, M., et al. “Planning for the Progressive Control of Foot-and-Mouth Disease Worldwide.” Transboundary and Emerging Diseases, Vol. 55, 2008, pp. 73–87. Sayler, C. “Border Makes New Mexico Vulnerable.” New Mexican, 25 March 2001.



Schat, K. A., and E. Baranowski. “Animal Vaccination and the Evolution of Viral Pathogens.” Revue Scientifique et Technique, Vol. 26, 2007, pp. 327–338. “Second Outbreak of Foot-and-Mouth Disease Confirmed in Britain.” CNN, 7 August 2007. Sobrino, F., et al. “Foot-and-Mouth Disease: A Long Known Virus, But a Current Threat.” Veterinary Research, Vol. 32, 2001, pp. 1–30. “Soil from Government Lab Linked to Disease.” United Press International, 14 December 2007. Ugarte, R. “Strategy for the Control of Foot-and-Mouth Disease in Uruguay.” Developments in Biologicals, Vol. 119, 2004, pp. 415–421.

ANTHRAX Summary of Threat Just the name says it all—but remember that anthrax is primarily a disease of cattle and other livestock. The agent is a bacterium that causes symptoms in cattle ranging from fever and convulsions to sudden death. In humans, anthrax more often presents as either a black scab on the skin or severe lung disease. Anthrax is classified as a biosecurity threat under the Bioterrorism Protection Act of 2002.

Other Names Anthrax was once called woolsorter’s disease, because it was an occupational hazard in the wool and hide industries. Other names are malignant pustule, malignant carbuncle, malignant edema, rag-picker’s disease, splenic fever, black bane, black blood, Siberian pest, and Siberian ulcer. Anthrax is called anthrax in many languages. It is also known as Milzbrand (“spleen fire”) in German, pernarutto (“spleen plague”) in Finnish, and charbon (“coal”) in French. The Greek word anthrax, which also means “coal,” refers to the black lesions. After the 2001 anthrax mailings, the media called the disease “thrax” for short. Soon “thrax” became a verb, meaning to infect with anthrax. This ghastly neologism evolved into the slang term “thraxed,” which, according to the Dictionary of American Slang, refers to an unfortunate state of affairs, often followed by “yo.”

Description The agent of anthrax is a spore-forming bacterium called Bacillus anthracis (Figure 4.4) that can infect most mammals. The symptoms and course of the disease depend on the mode of transmission (usually by contact, fomites, or ingestion) and the species. Infected cattle may have fever, convulsions, and breathing difficulty, or they may appear normal until shortly before death. Bleeding from orifices may also occur. The incubation period is usually 3 to 7 days for herbivores and 1 to 2 weeks for pigs. Most infections in ruminants and horses are fatal, but pigs and carnivores often recover. Most cattle are vaccinated in developed nations, but as of 2009, anthrax remains endemic in the Middle East, Africa, Central America, and South America. Sporadic cases and small outbreaks still occur in the United States, particularly in the southern Mississippi River Valley. Anthrax spores can survive in soil for many years.



Figure 4.4 Bacillus anthracis, the bacterium that causes anthrax. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

Which Animals Are at Risk? Most domesticated and wild herbivorous mammals are at risk for anthrax. In 2004, it killed several hundred hippopotami in Uganda. Unvaccinated cattle, sheep, goats, camels, horses, and pigs are all susceptible; carnivores, great apes, and humans are incidental hosts. Birds are resistant (Case Study 4-3). Case Study 4-3: Cold Chicken Risk may be highest in areas of neutral to Birds apparently are not susceptible to mildly alkaline soil with periods of flooding folanthrax because their body temperature is lowed by drought. Flooding brings the spores to too high for the bacteria to survive. We the surface of the ground, and drought exposes owe this discovery (among others) to them to grazing animals. Anthrax usually infects Louis Pasteur, who did a famous experihumans only in specific situations, such as wool ment in 1878. When he exposed a chicken processing plants and secret government labs. to anthrax and then chilled it in a basin of Sporadic cases of cutaneous anthrax, and a few cold water, the chicken developed anthrax fatal pulmonary infections, have resulted from and died. (Thraxed, yo.) But if he exposure to imported wool or hides. retrieved the chicken from the basin and warmed it up before it became too sick, it Some sources claim that vultures reduce recovered. anthrax risk by eating cows that die of anthrax before they rot and release spores. Others claim



that vultures increase risk by transporting infected material. Yet others report that vultures are becoming extinct anyway, because cow carcasses often contain high levels of toxic veterinary drugs.

The Numbers In 1945, more than 1 million sheep reportedly died from anthrax in Iran. In 1963, an anthrax outbreak killed an estimated 200 to 300 deer on an island in the Mississippi River in the United States, representing 60 to 90 percent of the herd. Global numbers are more readily available for humans; there are about 7,000 reported cases of human anthrax each year worldwide. The largest confirmed human outbreak was in Zimbabwe in 1979–1980, with 10,000+ cutaneous cases and at least 182 deaths. The largest known outbreak of human gastrointestinal anthrax was in Haiti in 1770, with 15,000 deaths. In humans, the death rate for untreated inhalation anthrax is close to 100 percent, but more than half of infected persons survived with prompt treatment in the 2001 postal outbreak. About 95 percent of all human anthrax cases are the cutaneous form, which is less dangerous; 20 percent of untreated cases may be fatal. History Several ancient authors, including Virgil (70–19 B.C.), described livestock diseases that sound like anthrax. One of the plagues of Egypt in the Old Testament may be a reference to anthrax. But the actual “discovery” of anthrax came much later, probably in the 1700s. Until then, farmers often regarded anthrax, rinderpest, and FMD as aspects of one great plague. In 1727, French physician Nicolas Fournier (1700–1781) described the forms of anthrax and its modes of transmission. In 1876, anthrax became the first disease linked to a microbial agent, thanks to the work of German physician Robert Koch (1843–1910). Louis Pasteur (1822–1895) developed the first anthrax vaccine for livestock in 1881. Prevention and Treatment Preventing anthrax requires annual vaccination of all grazing animals and postexposure prophylaxis of exposed animals. Adherence to reporting and quarantine measures, burning or burial of carcasses, and appropriate sanitary measures are essential. Antibiotics should not be given within the first week after the live vaccine. Human anthrax vaccines require multiple doses and annual boosters, and their routine use is controversial. In 2007, Scripps Research Institute announced a combined anthrax vaccineantitoxin that provides rapid treatment and long-term immunity with a single injection. Antibiotics often are effective if given within two days after exposure, either alone or in combination with a procedure to drain fluid from the chest. Popular Culture In the 1947 motion picture Stallion Road, a veterinarian named Larry (portrayed by Ronald Reagan) becomes infected with anthrax after treating diseased horses. A female rancher saves Larry by injecting him with the same antiserum he used on her horses, and they get married. Thus



the repentant old doctor who had given him up for dead gets the line that will ultimately shape Larry’s career: “All great progress has been made by unscientific people, mostly.” Larry later becomes Governor of California and president of the United States. In the 1939 motion picture Home on the Prairie, Texas Ranger Gene Autry tries to control an anthrax epidemic after the bad guys knowingly transport diseased cattle across the Mexican border into the United States. Some television westerns in the mid-1960s, including The Big Valley, also referred to anthrax as a disease of cattle. The same theme has appeared in several western novels, such as Dixon’s Edge, by Dennis O’Keefe (2001), in which a rancher is told that his cattle have anthrax and must be slaughtered. In 1981, two guitarists formed a heavy metal band that they called Anthrax, because it was the most evil-sounding name they could find in a biology book.

The Future As more countries adopt livestock management standards that prevent outbreaks of anthrax, it may join smallpox on the short list of deadly diseases that are of interest only to biodefense researchers and bioterrorists (Chapter 6).

References and Recommended Reading “Anthrax Epidemic Kills Man and Cows.” New York Times, 17 July 1909. Bakalar, N. “Discovering What Works on Anthrax.” New York Times, 21 February 2006. Banks, D. J., et al. “New Insights into the Functions of Anthrax Toxin.” Expert Reviews in Molecular Medicine, Vol. 8, 2006, pp. 1–18. Bullock, D. S. “Vultures as Disseminators of Anthrax.” Auk, Vol. 73, 1956, pp. 283–284. Clegg, S. B., et al. “Massive Outbreak of Anthrax in Wildlife in the Malilangwe Wildlife Reserve, Zimbabwe.” Veterinary Record, Vol. 160, 2007, pp. 113–118. Fasanella, A., et al. “Anthrax in Red Deer (Cervus elaphus), Italy.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1118–1119. Himsworth, C. G. “Anthrax in Saskatchewan 2006: An Outbreak Overview.” Canadian Veterinary Journal, Vol. 49, 2008, pp. 235–237. Hugh-Jones, M. E., and V. de Vos. “Anthrax and Wildlife.” Revue Scientifique et Technique, Vol. 21, 2002, pp. 359–383. Kellogg, F. E., and A. K. Prestwood. “Anthrax Epizootic in White-Tailed Deer.” Journal of Wildlife Diseases, Vol. 6, 1970, pp. 226–228. Leendertz, F. H., et al. “Anthrax in Western and Central African Great Apes.” American Journal of Primatology, Vol. 68, 2006, pp. 928–933. Meroney, J. “Ronald Reagan’s Anthrax Encounter.” Washington Post, 11 November 2001. Morens, D. M. “Characterizing a ‘New’ Disease: Epizootic and Epidemic Anthrax, 1769–1780.” American Journal of Public Health, Vol. 93, 2003, pp. 886–893. Nishi, J. S., et al. “An Outbreak of Anthrax (Bacillus anthracis) in Free-Roaming Bison in the Northwest Territories, June–July 2006.” Canadian Veterinary Journal, Vol. 48, 2007, pp. 37–38. Odontsetseg, N., et al. “Anthrax in Animals and Humans in Mongolia.” Revue Scientifique et Technique, Vol. 26, 2007, pp. 701–710. Oncü, S., et al. “Anthrax—An Overview.” Medical Science Monitor, Vol. 9, 2003, pp. RA276–283. Onion, A. “Vultures on the Brink of Extinction.” ABC News, 18 January 2006. Selva, M. “Hippo Deaths Raise Fears of Anthrax Epidemic.” The Independent, 12 November 2004. Shadomy, S. V., and T. L. Smith. “Zoonosis Update: Anthrax.” Journal of the American Veterinary Medical Association, Vol. 233, 2008, pp. 63–72. Stratidis, J., et al. “Cutaneous Anthrax Associated with Drum Making Using Goat Hides from West Africa— Connecticut, 2007.” Morbidity and Mortality Weekly Report, Vol. 57, 2008, pp. 628–631.



RINDERPEST Summary of Threat Rinderpest is a highly contagious cattle disease that has caused large epidemics. The virus is closely related to the human measles virus. WHO may soon declare rinderpest the second disease (after smallpox) that man has eradicated from the Earth. In 2009, it remains on the list of biosecurity threats designated under the Bioterrorism Protection Act of 2002. Other Names Rinderpest means “cattle plague” in German. English names include cattle plague, Russian cattle plague, steppe murrain, cattle murrain, contagious bovine typhus, and RPV (rinderpest virus). Names in most other languages translate as “cattle plague.” An 1871 book lists 121 names for rinderpest in India alone; the name used in Bombay, for example, meant “the great disease” or “the worst disease.” Wherever cattle represented wealth or security, rinderpest was greatly feared. It has sometimes been confused with a viral disease of sheep called ovine rinderpest or peste des petits ruminants. Description Rinderpest is (or was) among the worst of all cattle diseases. The death rate is high, and the disease spreads easily by contact or close-range airborne transmission. Cattle are the main hosts, but rinderpest can also infect sheep, goats, pigs, and many wild mammals. It was once prevalent in Europe and Africa, but it never became established in the New World, Australia, or New Zealand. Symptoms include fever, discharge from the eyes and nose (Figure 4.5), lesions in the mouth, breathing difficulty, and diarrhea. Loss of appetite, decreased milk yield, and abortion of calves may also occur. There is only one known serotype, and at least two of its three lineages have been eradicated.

Figure 4.5 A cow with rinderpest, showing increased lacrimation (runny eyes). Source: CSIRO Australian Animal Health Laboratory.



Which Animals Are at Risk? Cattle that have never been vaccinated or exposed to the rinderpest virus are at highest risk. The zebu, an African cattle breed, appears to have partial resistance. Sheep, goats, pigs, and hippopotami are only mildly susceptible, and the disease is rare in camels. There are no credible reports of humans contracting rinderpest. The Numbers The number of cases of classical wild-type rinderpest reported in 2003–2008 appears to be zero, although pockets of infection may remain in Somalia and adjacent countries. In past epidemics, rinderpest infected hundreds of millions of cattle, and the case fatality rate ranged from about 20 percent to 90 percent. History In 1889–1896, rinderpest killed about 90 percent of cattle and many wild mammals in Africa, causing great hardship. In 2000, a conservationist wrote: “This animal pandemic could easily be the greatest catastrophe ever to strike the continent, rivaling that of the AIDS virus that is today decimating the population of this hapless land.”1 The pandemic (technically a panzootic) might have resulted from contact with infected Russian or Italian cattle, exacerbated by hot weather that forced animals to crowd together at water holes. Early vaccination methods were largely unsuccessful (Case Study 4-4). From 1969 to 1997, rinderpest swept Case Study 4-4: A Long Time Coming through the Middle East, killing a large percentage of cattle in Iran, Iraq, Turkey, Lebanon, In 1754 an anonymous correspondent to Syria, Israel, and the Arabian Peninsula. But Gentleman’s Magazine reported that he thanks to an aggressive eradication campaign, all had successfully inoculated nine out of ten cattle against rinderpest by dipping a cloth these countries were free of rinderpest by the end in body fluids from an infected animal and of 1999. Several countries initiated such caminserting the cloth into an incision in the paigns in 1987, and in 1993 the United Nations dewlap of a healthy animal. A series of coordinated these efforts under its aegis. similar experiments continued in several Unlike smallpox, rinderpest infects many European countries during the eighteenth species, including wild hosts that must also be and nineteenth centuries, but a fully effectested. Civil unrest in Africa has further complitive vaccine did not become available until cated the problem, by disrupting governments and after 1956, when British veterinarian Walincreasing demand for meat. The vaccine is hard to ter Plowright (1923– ) used cell cultures to deliver to remote areas in Africa because it breaks develop a live attenuated rinderpest virus. down in hot weather. Despite these problems, it In 1999, Dr. Plowright won the World Food Prize for this achievement. appears that mass vaccination and improved public relations have finally done the trick.

Prevention and Treatment Methods used to control past outbreaks include ring vaccination (using the attenuated cell culture vaccine), sometimes in combination with a slaughter program. Valuable animals were 1. Smithsonian Institution Digital Repository: Letter from the Desk of David Challinor, October 2000.



saved with supportive care and antibiotics to control secondary bacterial infections. Animals that recovered had long-lasting immunity.

Popular Culture An engraving by François-Hippolyte Lalaisse (1812–1884), entitled “The Plague of the Cattle Murrain,” shows dead cattle and distraught farmers in the aftermath of a European rinderpest outbreak. An 1866 British diarist wrote: “The cattle plague is spreading through the county like a roaring lion seeking whom it may devour. Some say it is a Russian disease, they call it the Renderpest.”2 The result of Africa’s 1889 rinderpest tragedy is visible in every Hollywood movie that depicts big game hunters hiring African porters in that era. The otherwise unaccountable supply of cheap, compliant labor represented cattle farmers who had recently lost their herds to rinderpest. According to Masai tradition, a medicine man named Mbatian predicted the cattle plague: He told the people to move their grazing grounds, “for,” he said, “all the cattle will die. You will first of all see flies which make hives like bees, then the wild beasts will die, and afterwards the cattle.” Both of these prophesies have come true: the Europeans have arrived, and the cattle died. Mbatian himself died while the cattle plague was raging (circa 1890).3

This unpleasantly Borg-like image of swarms of hive-building flies apparently refers to European colonists. (Another Masai tradition described them as green-skinned aquatic creatures with fat in their veins instead of blood.) The famous Tsavo Man-Eaters—two lions that killed and ate numerous railway workers in Kenya in 1898—quite possibly resorted to snacking on humans because rinderpest had killed most of their usual prey, such as cattle and buffalo. Others have proposed that the lions had broken teeth that impaired their hunting ability. Nearly a century later, director Stephen Hopkins and screenwriter William Goldman immortalized this event in the 1996 motion picture The Ghost and the Darkness.

The Future We are happy to report that the rinderpest virus may have no future, except in a few secure government freezers, alongside smallpox and other horrors of the past that may soon join them. But celebration may be premature. Rinderpest was nearly eradicated once before, in the mid1970s, only to return after some nations relaxed their surveillance and vaccination programs.

References and Recommended Reading Barrett, T., and P. B. Rossiter. “Rinderpest: the Disease and Its Impact on Humans and Animals.” Advances in Virus Research, Vol. 53, 1999, pp. 89–110. Center for Food Security and Public Health. “Rinderpest.” Iowa State University College of Veterinary Medicine, updated August 2008.

2. Journal of John Ostle, January 1866. 3. Hollis, A.C. 1905. The Masai: Their Language and Folklore. Oxford: Clarendon Press.



DeClerc, K., and N. Goris. “Extending the Foot-and-Mouth Disease Module to the Control of Other Diseases.” Developments in Biologicals, Vol. 119, 2004, pp. 333–40. Diop, B. A., and P. Bastiaensen. “Achieving Full Eradication of Rinderpest in Africa.” Veterinary Record, Vol. 157, 2005, pp. 239–240. Matin, M. A., and M. A. Rafi. “Present Status of Rinderpest Diseases in Pakistan.” Journal of Veterinary Medicine B, Infectious Diseases and Veterinary Public Health, Vol. 53, Supplement 1, 2006, pp. 26–28. Mills, C. “The Wild, Wild Pest.” The Sciences, March/April 1999. Mukhopadhyay, A. K., et al. “Rinderpest: a Case Study of Animal Health Emergency Management.” Revue Scientifique et Technique, Vol. 18, 1999, pp. 164–178. Normile, D. “Rinderpest: Driven to Extinction.” Science, Vol. 319, 2008, pp. 1606–1609. Roeder, P. L., et al. “Experience with Eradicating Rinderpest by Vaccination.” Developments in Biologicals (Basel), Vol. 119, 2004, pp. 73–791. Roeder, P. L., and W. P. Taylor. “Rinderpest.” Veterinary Clinics of North America Food Animal Practice, Vol. 18, 2002, pp. 515–547. Rossiter, P., et al. “Rinderpest Seroprevalence in Wildlife in Kenya and Tanzania, 1982–1993.” Preventive Veterinary Medicine, Vol. 75, 2006, pp. 1–7. Spinage, C. A. 2003. Cattle Plague: A History. Philadelphia: J. B. Lippincott. Tambi, E. N., et al. “Economic Impact Assessment of Rinderpest Control in Africa.” Revue Scientifique et Technique, Vol. 18, 1999, pp. 458–477. Taylor, W. P., et al. “The Principles and Practice of Rinderpest Eradication.” Veterinary Microbiology, Vol. 44, 1995, pp. 359–367.

HEARTWATER Summary of Threat Heartwater is a deadly tick-borne disease of cattle, sheep, goats, and other animals, possibly including humans. Symptoms vary by species. The agent is a rickettsia (similar to a bacterium) that can live only as a parasite inside cells. As of 2009, heartwater has not reached North America, but it is listed as a biosecurity threat under the Bioterrorism Protection Act of 2002.

Other Names Heartwater is also called cowdriosis, ehrlichiosis (one of several forms), or Ehrlichia ruminantium infection. Names in other languages include malkopsiekte or bossiekte (Afrikaans), hidropericardio (Spanish), péricardite exsudative infectieuse (French), hidrocarditis infecciosa (Portuguese), and idropericardite dei ruminanti (Italian). The Xhosa people of South Africa reportedly call this disease inyongo.

Description As of 2009, heartwater is endemic in sub-Saharan Africa and offshore islands and has also reached several Caribbean islands. The agent (Ehrlichia ruminantium) belongs to a group of small bacteria-like organisms called rickettsiae that can live and reproduce only as parasites inside living cells. Most rickettsial diseases depend on ticks or other arthropod vectors, not only to transmit them between hosts but also to serve as hosts during part of the life cycle (Case Study 4-5). Heartwater vectors include the tropical bont tick (Amblyomma variegatum) and


related species (Figure 4.6). The female bont tick, about the size of a grape when fully engorged, can also inflict severe bite wounds. Symptoms are variable but often include fever, loss of appetite, convulsions, and prostration. Heartwater causes the blood vessels to become more permeable, and fluid or blood may collect in the lungs or in the pericardial sac, which surrounds the heart. Animals that recover may become carriers.

Which Animals Are at Risk? Domestic cattle, sheep, and goats infected with heartwater become severely ill, but some other mammals, birds, and reptiles can carry the disease without showing signs. Heartwater has turned up in many species including Cape buffalo, giraffe, antelope, deer, guinea fowl, ostrich, and leopard tortoise. Studies suggest that heartwater can also infect dogs and possibly humans.


Case Study 4-5: The Life of a Tick The tropical bont tick (TBT) is an example of a three-host tick. The female lays up to 20,000 eggs on the ground, where they hatch into groups of larvae that ascend blades of grass and wait. When these larvae sense the presence of a suitable host, they attach themselves to its muzzle or legs and feed on blood. The TBT at this stage prefers hairy parts of mammals, their principal hosts, but in a pinch they will accept a reptile or bird instead. Once engorged, the larvae drop to the ground and molt into nymphs, which then attach to a second host. The engorged nymphs again drop to the ground and molt into brightly colored adult ticks. The male TBT ascends the third host and often attaches near its anus, where he secretes a chemical that attracts the female tick. She climbs up and joins him, they mate, she becomes engorged with blood and drops to the ground, and the cycle starts over.

Figure 4.6 A female gulf coast tick (Amblyomma maculatum), one of the known vectors of heartwater. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



The Numbers According to the U.S. Department of Agriculture, if heartwater reaches the United States, it could cost the livestock industry at least $762 million per year. Since livestock in North America has no acquired resistance to this disease, and no vaccine is yet available, the mortality rate could approach 100 percent. In countries such as Zimbabwe, where heartwater is endemic, the largest component of economic loss is the cost of acaricides (tick-killing agents) and the dipping process used to kill ticks. Other costs include the loss of animals, their milk and other products and the cost of treatment.

History British veterinarians who investigated heartwater in South Africa in the 1800s found that local settlers had beaten them to it. The ranchers already knew that bont ticks had arrived in the 1830s and somehow caused heartwater; they also knew heartwater was related to vegetation density, elevation, and overstocking. But the vets rejected these explanations in favor of a soil-borne anthrax-like agent, although the blood of animals with heartwater contained no bacteria that were visible using the instruments of the day. Thus, the researchers imported a batch of Pasteur’s new anthrax vaccine and administered it to sheep, several of which promptly contracted anthrax and died. The study ended in frustration, and the team went home. The role of ticks did not become clear until American scientists published a study of babesiosis in the 1890s. In 1900, South African scientists successfully infected a goat with heartwater, infested it with bont ticks, and then transferred the ticks to healthy goats, which soon developed heartwater. Koch’s Postulates were fulfilled, and the mode of transmission was known, although the heartwater agent remained elusive until 1925 because of its small size.

Prevention and Treatment As of 2009, no commercial heartwater vaccine is available. Studies of attenuated and recombinant vaccines are in progress, but these vaccines have not been fully validated under field conditions. Antibiotics such as tetracycline may be effective, but only at the earliest stages of the disease. In some African countries, farmers induce a controlled heartwater infection by exposing cattle to infected sheep blood, then monitor the animals’ body temperature and give them antibiotics if necessary. Corticosteroids have also been used as supportive therapy. Control of tick infestation (by dipping animals or spraying brush) may help prevent infection, but excessive reduction of tick numbers may backfire by interfering with maintenance of adequate immunity. A 1989 study showed that bont ticks prefer cows that male bont ticks have already visited, because the previous tick deposits a pheromone that labels the cow as a suitable meal. The downside is that ticks may avoid cattle that have been treated with acaricides. Also, treated cattle may gradually lose their immunity and later develop severe disease when exposed again.

Popular Culture The Xhosa people of South Africa use several herbal remedies to treat their livestock for heartwater, including the bark of Cape lancewood (Curtisia dentata), red beech (Protorhus longifolia),



Cape beech (Rapanea melanophloeos), and false horsewood (Hippobromus pauciflorus); the root bark of kerriebossie (Gnidia capitata); the tuber of geranium (Pelargonium reniforme); and the climbing stem of swart teebossie (Vernonia mespilifolia). Traditional methods of tick removal have evolved into urban legends that are best ignored. If you burn the tick with a match, poison it with gasoline, or cover it with nail polish or liquid soap or petroleum jelly, it may regurgitate infected material into the wound. It may also die, leaving its mouthparts embedded in the skin, where an infection or granuloma may develop. The best way to remove an attached tick (from a person or animal) is to grasp the tick lightly, just behind its head—using tweezers, a loop of thread, a tick extractor, or two fingernails—and pull it straight out, slowly. Don’t decapitate the tick or squeeze its body, and don’t stop pulling until the tick lets go. Then kill it.

The Future Birds called cattle egrets often carry tropical bont ticks, the vectors of heartwater. Cattle egrets are already common in North America, but bont ticks are not; the question is whether infested egrets can make the journey. And the answer is yes—otherwise, we would not have chosen this example. In 1990, researchers marked cattle egrets on Caribbean islands where heartwater exists, and tracked one of these birds to the Florida Keys. Tortoises and other reptiles imported from Africa as pets are also a source of worry, since they, too, can carry bont ticks. These facts suggest that heartwater will reach North America sooner or later.

References and Recommended Reading Allan, S. A., et al. “Ixodid Ticks on White-Tailed Deer and Feral Swine in Florida.” Journal of Vector Ecology, Vol. 26, 2001, pp. 93–102. Allsopp, M. T., et al. “Novel Ehrlichia Genotype Detected in Dogs in South Africa.” Journal of Clinical Microbiology, Vol. 39, 2001, pp. 4204–4207. Allsopp, M. T., et al. “Ehrlichia ruminantium: An Emerging Human Pathogen?” Annals of the New York Academy of Sciences, Vol. 1063, 2005, pp. 358–360. Anderson, P. G. 2007. “Edmund Vincent Cowdry (1888–1975).” St. Louis, MO: Bernard Becker Medical Library, Washington University School of Medicine. APHIS Veterinary Services. 2002. “Heartwater Factsheet.” U.S. Department of Agriculture, July 2002. Burridge, M. J. “Ticks (Acari: Ixodidae) Spread by the International Trade in Reptiles and Their Potential Roles in Dissemination of Diseases.” Bulletin of Entomological Research, Vol. 91, 2001, pp. 3–23. Burridge, M. J., et al. “Increasing Risks of Introduction of Heartwater onto the American Mainland Associated with Animal Movements.” Annals of the New York Academy of Sciences, Vol. 969, 2002, pp. 269–274. Center for Food Security and Public Health. “Heartwater.” Factsheet, Iowa State University College of Veterinary Medicine, updated 28 September 2007. Cocks, M. L., and A. P. Dold. “Cultural Significance of Biodiversity: The Role of Medicinal Plants in Urban African Cultural Practices in the Eastern Cape, South Africa. Journal of Ethnobiology, Vol. 26, 2006, pp. 60–82. Gilfoyle, D. “The Heartwater Mystery: Veterinary and Popular Ideas about Tick-Borne Animal Diseases at the Cape, c. 1877–1910.” Kronos: The Journal of Cape History, Vol. 29, 2003, pp. 139–160. “Imported Ticks Can Pose Threat to Florida Herds.” Associated Press, 29 October 1989. Jancin, B. “Plucking at Myths Surrounding Tick Removal.” Family Practice News, 1 November 2000.



Loftis, A. D., et al. “Infection of a Goat with a Tick-Transmitted Ehrlichia from Georgia, U.S.A., That Is Closely Related to Ehrlichia ruminantium.” Journal of Vector Ecology, Vol. 31, 2006, pp. 213–223. Loftis, A. D., et al. “Geographic Distribution and Genetic Diversity of the Ehrlichia sp. from Panola Mountain in Amblyomma americanum.” BMC Infectious Diseases, 23 April 2008. Louw, M., et al. 2005. “Ehrlichia ruminantium, an Emerging Human Pathogen—A Further Report.” South African Medical Journal, Vol. 95, 2005, pp. 948–949. Mahan, S. M., et al. “Development of Improved Vaccines for Heartwater.” Developments in Biologicals (Basel), Vol. 114, 2003, pp. 137–145. “Ostriches Barred Entry.” Associated Press, 6 July 1989. Pedregal, A., et al. “Toward Prevention of Cowdriosis.” Annals of the New York Academy of Sciences, Vol. 1149, 2008, pp. 286–291. Peter, T. F., et al. “Ehrlichia ruminantium Infection (Heartwater) in Wild Animals.” Trends in Parasitology, Vol. 18, 2002, pp. 214–218. Provost, A., and J. D. Bezuidenhout. “The Historical Background and Global Importance of Heartwater.” Onderstepoort Journal of Veterinary Research, Vol. 54, 1987, pp. 165–169. Reeves, W. K., et al. “The First Report of Human Illness Associated with the Panola Mountain Ehrlichia Species: a Case Report.” Journal of Medical Case Reports, 30 April 2008. Shkap, V., et al. “Attenuated Vaccines for Tropical Theileriosis, Babesiosis and Heartwater: The Continuing Necessity.” Trends in Parasitology, Vol. 23, 2007, pp. 420–426. “Specialist Warns Against Foreign Ticks.” Gazette-Enterprise (Texas), 23 July 2000. “Ticks Follow Fellows to Tastiest Cows.” Science News, 25 February 1989. Wagner, G. G., et al. “Babesiosis and Heartwater: Threats Without Boundaries.” Veterinary Clinics of North America Food Animal Practice, Vol. 18, 2002, pp. 417–430. Yabsley, M. J., et al. “Natural and Experimental Infection of White-Tailed Deer (Odocoileus virginianus) from the United States with an Ehrlichia sp. Closely Related to Ehrlichia ruminantium.” Journal of Wildlife Diseases, Vol. 44, 2008, pp. 381–387. Yunker, C. E. “Heartwater in Sheep and Goats: a Review.” Onderstepoort Journal of Veterinary Research, Vol. 63, 1996, pp. 159–170.

CLASSICAL SWINE FEVER Summary of Threat Classical swine fever (CSF) is a highly contagious viral disease that has caused large epidemics and major financial losses. Hosts include domestic pigs and wild boars. The actual death rate is low for most modern CSF virus strains, but controlling outbreaks may require culling large number of pigs. This disease is classified as a biosecurity threat under the Bioterrorism Protection Act of 2002.

Other Names Classical swine fever is also called hog cholera, and the classical swine fever virus (CSFV) is also called hog cholera virus (HCV). Less common names are pig typhoid, pig plague, swine plague, Billings’ swine plague, swine pest, pneumoenteritis of swine, swine diphtheritis, and infectious pneumonia of swine. Names in other languages include peste porcina clásica or cólera porcina (Spanish), peste suína clássica (Portuguese), peste du porc (French), sikarutto (Finnish), Virusschweinepest (German), and klassieke varkenspest (Dutch).



Media references to “swine fever” may lead to confusion with African swine fever, a different disease that (as of 2009) has never been found in the United States. The name “hog cholera” also refers to at least two other diseases of swine.

Description The agent is a small RNA virus in the family Flaviviridae, a group that also includes the agents of dengue fever and hepatitis C in humans. CSF spreads by contact with infected animals or contaminated surfaces, insemination or other exchange of body fluids, close-range airborne or aerosol transmission, and possibly by flying insects, lice, and various small animals. Symptoms include high fever, convulsions, loss of appetite, a depressed appearance, and the tendency of pigs to huddle together (Figure 4.7). Diarrhea, breathing difficulty, and eye irritation may occur. Pigs infected with a virulent strain often die within a week or two. Those with chronic CSF may survive for a few months, or else recover and then suffer a fatal relapse. Survivors often have smaller litters, stillbirths, or high mortality at weaning. As of 2009, classical swine fever remains a deadly disease partly because of international policy. To export pigs, a nation must prove that its pigs are free of CSF antibodies. But since vaccination produces antibodies that are indistinguishable from those resulting from infection, the only economically feasible way to stop an outbreak is by slaughtering pigs.

Figure 4.7 Depression is an early symptom of classical swine fever. Source: Frank Filippi, CSIRO Australian Animal Health Laboratory.



Which Animals Are at Risk? The only known hosts for classical swine fever are pigs (including wild boars), although other animal species can be infected experimentally. If exposed, all unvaccinated pigs are at risk.

The Numbers In 1997–1998, a classical swine fever epidemic in the Netherlands resulted in the deaths of about 11 million pigs. Only about 10 percent of those pigs died from the disease itself; the rest were slaughtered to stop the outbreak while maintaining disease-free status according to European Union policy. Estimates of the resulting losses to the swine industry range from $2.3 billion to $5 billion in U.S. dollars.

History Classical swine fever first appeared in Indiana sometime before 1833 and was a major threat to swine production until 1962, when Public Law 87-209 started a vaccination campaign that eliminated CSF from the United States by 1977. As of 2009, the United States remains free of this disease. A compulsory slaughter program in the United Kingdom eliminated the disease in 1966, but minor outbreaks occurred in 1971, 1986, and 2000. The last outbreak in England closely followed the epidemics of mad cow disease and foot-and-mouth disease, and the result was a temporary reduction of consumer confidence in British food.

Prevention and Treatment Live attenuated vaccines are commercially available, but they make it hard to detect circulating viruses. Maternal antibodies may also interfere with the induction of immunity. “Marker” vaccines allow discrimination between infected and vaccinated pigs, but these vaccines are less effective than live vaccines, and the diagnostic test also has limitations. As a result, most developed nations prohibit vaccination in CSF-free areas, and they control outbreaks by slaughtering confirmed cases and contacts. Wild boars and feral pigs might serve as a reservoir for classical swine fever, but it would not be feasible to test or kill all of them. The EU has used a combination of oral vaccines and hunting to control disease in wild boars.

Popular Culture American journalist Stephen Bonsal’s 1937 memoir Heyday in a Vanished World relates how the Dual Monarchy of Austria and Hungary barred Serbian pigs after some were found with hog cholera. But since Serbian pigs were not considered edible until they had fattened on Hungarian pastures, the export ban resulted in starvation for swine and swineherds alike, despite the press of swine in the streets of Belgrade. Some people have claimed that the USDA inspection marks stamped on supermarket meat represent the “number of the beast,” or that the indelible purple dye is poisonous. In fact, this


harmless vegetable dye was the invention of Dr. Marion Dorset, the same USDA scientist who identified the agent of classical swine fever and developed the vaccine (Case Study 4-6). A book on Native American herbal medicine states that the Meskwaki people fed their pigs the root of the feathery false Solomon’s seal plant (Smilacina racemosa) to prevent hog cholera or classical swine fever. Since this disease first reached North America in the early 1800s, the practice was not an ancient one. German farmers once believed that pigs would not contract hog cholera if they were treated for seven days with water containing a plant called asphodel (probably Asphodelus ramosus). In ancient Europe, this plant was sacred to the goddess Persephone, whose worship involved the sacrifice of pigs.

The Future Regardless of how the reader (or author) may feel about animal rights issues, recent events have made it clear that significant numbers of people worldwide oppose the mass slaughter of pigs or cattle for disease control purposes. Thus, an alternative course of action will most likely present itself in the near future. An improved marker vaccine might satisfy both public health and ethical concerns.


Case Study 4-6: The Legacy of Dr. Marion Dorset USDA researcher Marion Dorset (1872–1935) was responsible for the conquest of hog cholera in the United States. He also studied bovine TB and other animal diseases, and colleagues compared his work to that of Pasteur and Koch, yet Dr. Dorset was renowned for his dedication and modesty. His obituary states, in part: On the occasion of his discovery of anti-hog cholera serum, Doctor Dorset had the opportunity to acquire wealth through the manufacture and sale of this product for which a large demand promptly developed. But after applying for and receiving a patent [No. 1,784,928], he gave it to the government and to the public so that any person in the United States might use the method without payment of royalty.*

Nor did his legacy end with his death in 1935. His son Virgil “Jack” Dorset became a physician and volunteered for service in Manila in World War II, only to be captured at the fall of Bataan. He continued his role as medical officer in the prison camps and, in 1944, was moved to a camp in Japan, where he witnessed the cloud from the atomic bomb at Nagasaki. After the camp was liberated, Col. Dorset became a surgeon in the U.S. Marine Hospital. He died in Texas in 1999, a hero in the best tradition. *

Wyoming Stockman-Farmer, 1 August 1935.

References and Recommended Reading Artois, M., et al. “Classical Swine Fever (Hog Cholera) in Wild Boar in Europe.” Revue Scientifique et Technique, Vol. 21, 2002, pp. 287–303. Blome, S., et al. “Assessment of Classical Swine Fever Diagnostics and Vaccine Performance.” Revue Scientifique et Technique, Vol. 25, 2006, pp. 1025–1038. Edwards, S., et al. “Classical Swine Fever: the Global Situation.” Veterinary Microbiology, Vol. 73, 2000, pp. 103–119. Greiser-Wilke, I., et al. “Diagnostic Methods for Detection of Classical Swine Fever Virus—Status Quo and New Developments.” Vaccine, Vol. 25, 2007, pp. 5524–5530. Luy, J., and K. R. Depner. “The Need for a Paradigm Shift in the Control of Classical Swine Fever.” EurSafe News, Vol. 8, 2006, pp. 3–6. Moennig, V., et al. “Clinical Signs and Epidemiology of Classical Swine Fever: A Review of New Knowledge.” Veterinary Journal, Vol. 165, 2003, pp. 11–20. Morilla, A., et al. (Eds.) 2002. Trends in Emerging Viral Infections of Swine. Ames: University of Iowa Press. Paton, D. J., and I. Greiser-Wilke. “Classical Swine Fever—An Update.” Research in Veterinary Science, Vol. 75, 2003, pp. 169–178.



Reynolds, D. “Vigilance for Classical Swine Fever and FMD.” Veterinary Record, Vol. 158, 2006, p. 383. Ribbens, S., et al. “Transmission of Classical Swine Fever. A Review.” Veterinary Quarterly, Vol. 26, 2004, pp. 146–155. Ribbens, S., et al. “Evidence of Indirect Transmission of Classical Swine Fever Virus through Contacts with People.” Veterinary Record, Vol. 160, 2007, pp. 687–690. Suradhat, S., et al. “Factors Critical for Successful Vaccination against Classical Swine Fever in Endemic Areas.” Veterinary Microbiology, Vol. 119, 2007, pp. 1–9. Terpstra, C., and A. J. de Smit. “The 1997/1998 Epizootic of Swine Fever in the Netherlands: Control Strategies Under a Non-Vaccination Regimen.” Veterinary Microbiology, Vol. 77, 2000, pp. 3–15. U.S. Department of Agriculture, Animal and Plant Health Inspection Service. “Procedure Manual for Classical Swine Fever (CSF) Surveillance.” Version 2.0, 1 April 2007. van Oirschot, J. T. “Diva Vaccines that Reduce Virus Transmission.” Journal of Biotechnology, Vol. 73, 1999, pp. 195–205. van Oirschot, J. T. “Emergency Vaccination against Classical Swine Fever.” Developments in Biologicals, Vol. 114, 2003, pp. 259–267.

BLUE-EAR PIG DISEASE Summary of Threat A mysterious viral disease caused great concern in 2007 when it killed an estimated 10 million pigs in China, but it later turned out to be the same as a disease first seen in North America in 1987. It mainly affects the respiratory and reproductive systems. As of 2009, there are no known hosts other than swine, although some wild animals have been infected experimentally. A commercial vaccine is available.

Other Names In the early 1990s, the media referred to this disease as “mystery swine disease” or MSD. It is now called blue-ear (or blue-eared) pig disease, porcine reproductive and respiratory syndrome (PRRS), porcine epidemic abortion and respiratory syndrome (PEARS), or porcine high fever disease (PHFD). Older names include swine infertility and respiratory syndrome (SIRS), new pig disease, pig plague of 1989, Wabash syndrome, and swine plague. The agent is Lelystad virus, porcine arterivirus, or PRRSV. Blue-ear pig disease is abortus blauw in Dutch, seuchenhafter Spätabort der Schweine or rätselhafte Schweinekrankheit in German, syndrom reproductif et respiratoire du porc in French, síndrome disgenésico y respiratorio del cerdo or enfermedad misteriosa del cerdo in Spanish, heko-heko in Japanese, and lan er bing in Chinese.

Description The agent is a small RNA virus in the family Arteriviridae. Symptoms may include encephalitis, heart problems, infertility, stillbirth, and late-term abortion in adult pigs, or severe pneumonia in piglets. The blue or purple discoloration that gives the disease its popular name occurs in only 1 to 2 percent of pigs, but the name has stuck (Figure 4.8).



Figure 4.8 Pigs suffering from porcine reproductive and respiratory syndrome (PRRS), also called blue-ear pig disease. Source: CSIRO Australian Animal Health Laboratory.

PRRS spreads mainly by direct contact with body fluids or contaminated surfaces, including the hands, clothing, or vehicles of swine workers. Flies and mosquitoes can also serve as mechanical vectors. The disease is present in North and South America, Asia, and most of Europe. As of 2009, only three countries (Australia, New Zealand, and Switzerland) are officially free of PRRS.

Which Animals Are at Risk? All domestic and wild pigs appear to be susceptible, but the death rate is highest among recently weaned pigs from infected litters. Older pigs often recover, but long-term effects may include immune suppression and secondary bacterial infections.

The Numbers The case fatality rate for PRRS is usually 10 to 20 percent for all age groups or 40 percent for piglets, not including losses from culling. The 2006–2007 epidemic in China killed an estimated 10 million pigs, but China is a big country; to put this number in perspective, China reportedly loses about 25 million pigs to all diseases in a typical year (see also Case Study 4-7, page XXX). The epidemic contributed to the economic impact from pork prices, which reportedly rose by about 75 percent in 2007.



Case Study 4-7: Strong Pig After the 2008 earthquake that devastated southwest China, a pig was found that had survived for 36 days buried under rubble, sustained only by rainwater and a bag of charcoal. The pig became China’s animal of the year and now lives in a museum. This event is noteworthy in a nation that lost some 10 million pigs to blue-ear pig disease the year before. Like Phoenix the Calf (Case Study 4-2), the Strong Pig (Zhu Jianqiang) became a symbol of hope and renewal that transcends cultural boundaries.

As of 2007–2008, PRRS infected about 60 percent of swine herds in the United States each year, and the annual economic impact of PRRS on pork producers in the United States alone was estimated to be $560 million to $762 million. In 2008, the Vietnamese government reported that three PRRS outbreaks had infected a total of 338,736 pigs and necessitated the slaughter of 288,000. Vietnam requested international help and imported vaccine from China.


First reported in the United States in 1987, “mystery swine disease” caused a series of epidemics in North America and Europe. Researchers in South Dakota, Minnesota, and Missouri identified the cause as a viral infection and began work on a vaccine. PRRS was pandemic by the early 1990s, and the first of several live virus vaccines became available in 1994. A swine disease that appeared in China in 2006 later turned out to be a highly virulent form of PRRS. Changes in swine production in the second half of the twentieth century, including increased transportation of live animals and sperm, may have facilitated the spread of this virus.

Prevention and Treatment As of 2009, no consistently effective treatment is available, but commercial vaccines (both live and killed) have helped to control outbreaks and reduce losses. These vaccines are not entirely effective because of the high genetic diversity of the virus. Other preventive measures are the same as for any disease: breed resistant strains, maintain surveillance programs, and keep pig farms reasonably clean. Swine workers should wash their hands and change clothes after handling infected pigs.

Popular Culture Since this disease was virtually unknown to the public until about 1991, it is too new to have permeated popular culture to any great extent. We know of no motion pictures or songs about this disease. In 2009, the website of an American man living in Vietnam displayed a photograph of a local bakery’s cake, topped with a miniature blue-eared pig sculpted in frosting, but this phenomenon is too recent to evaluate. The 2006–2007 PRRS epidemic did, however, start at least one Internet rumor. In 2008, after the press reported that the Chinese government tried to cover up the epidemic, suspicion grew that China might be endangering global health by its secrecy on issues such as SARS, bird flu, contaminated pet food, toxic drywall, hair bands made from recycled condoms, and lead-based paint. For some, the next logical step was to point out the bruised appearance of



“blue-eared pigs” and suggest that the Chinese were concealing an outbreak of hemorrhagic fever, possibly Ebola. The timing was good; in 2008, Ebola Reston and PRRS were found to coexist in Philippine pigs. Next, someone speculated that a recombinant Ebola virus had escaped from a Chinese lab, causing the human disease outbreak later blamed on Streptococcus suis (Chapter 3). In the next few years, these suspicions may coalesce into an elaborate conspiracy theory.

The Future After the 2007 outbreak, colloquium participants predicted that improved PRRS vaccines would be available within 5 to 10 years. Meanwhile, the Chinese government instituted a nationwide program to prevent future outbreaks. If other countries follow China’s example, blue-eared pigs may soon exist only in history books.

References and Recommended Reading Barboza, D. “Virus Spreading Alarm and Pig Disease in China.” New York Times, 16 August 2007. Beilage, E. G., and H. J. Batza. “PRRSV-Eradication: An Option for Pig Herds in Germany?” Berliner und Münchener Tierärztliche Wochenschrift, Vol. 120, 2007, pp. 470–479. [German] “Blue-Ear Pig Disease Discovered Nationwide.” China Daily, 12 June 2007. Chae, C. “A Review of Porcine Circovirus 2-Associated Syndromes and Diseases.” Veterinary Journal, Vol. 169, 2005, pp. 326–336. “China Arrests Makers of Fake Vaccine for Pig Disease.” Associated Press, 29 October 2007. Cho, J. G., and S. A. Dee. “Porcine Reproductive and Respiratory Syndrome Virus.” Theriogenology, Vol. 66, 2006, pp. 655–662. Collins, J. E., et al. “Isolation of Swine Infertility and Respiratory Syndrome Virus (Isolate ATCC VR-2332) in North America and Experimental Reproduction of the Disease in Gnotobiotic Pigs.” Journal of Veterinary Diagnostic Investigation, Vol. 4, 1992, pp. 117–126. Goyal, S. M. “Porcine Reproductive and Respiratory Syndrome.” Journal of Veterinary Diagnostic Investigation, Vol. 5, 1993, pp. 656–664. Hornby, L. “China Official Fired over Blue Ear Disease Outbreak.” Reuters, 11 February 2009. Keffaber, K. K. “Reproductive Failure of Unknown Etiology.” American Association of Swine Practitioners Newsletter, Vol. 1, 1989, pp. 1–10. Mateu, E., and I. Diaz. “The Challenge of PRRS Immunology.” Veterinary Journal, Vol. 177, 2008, pp. 345–351. Plagemann, P. G. “Porcine Reproductive and Respiratory Syndrome: Origin Hypothesis.” Emerging Infectious Diseases, Vol. 9, 2003, pp. 903–908. “Quake Zone Hero Pig Named China’s Animal of the Year.” Taipei Times, 29 December 2008. “Scientists Solve Part of Mystery Swine Disease.” Associated Press, 13 November 1991. “Swine Study Looks at Mutating Pig Virus.” United Press International, 21 February 2008. Terpstra, C., et al. “Experimental Reproduction of Porcine Epidemic Abortion and Respiratory Syndrome (Mystery Swine Disease) by Infection with Lelystad Virus: Koch’s Postulates Fulfilled.” Veterinary Quarterly, Vol. 13, 1991, pp. 131–136. Tong, G.-Z., et al. “Highly Pathogenic Porcine Reproductive and Respiratory Syndrome, China.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1434–1436. “USDA Renews Program to Fight Pig Syndrome.” United Press International, 24 July 2008. “Vietnam Hit by Outbreak of Blue-Eared Pig Disease.” China Post, 8 April 2006. Zimmerman, J. (Ed.). 2003. PRRS Compendium Producer Edition. Des Moines, IA: National Pork Board.



NEWCASTLE DISEASE Summary of Threat Newcastle disease (ND) is a deadly viral infection of chickens, turkeys, and other domestic and wild birds. The most virulent strains can quickly kill entire flocks. ND can also cause illness (usually mild) in humans. Vaccines are available for some strains. This highly contagious disease is classified as a biosecurity threat under the Bioterrorism Protection Act of 2002.

Other Names Newcastle disease, or ND, is also called New Castle disease (NCD), fowlpest, Doyle’s disease, Egyptian fowl-plague, Korean fowl-plague, Asiatic fowl-plague, pseudoplague, pseudo-poultry plague, avian distemper, Ranikhet disease, Tetelo disease, avian pneumoencephalitis, atypical Geflugelpest, or respiratory nervous disorder. Names of specific ND strains include virulent Newcastle disease (VND), Asiatic Newcastle disease (AND), velogenic neurotropic ND (VNND), and velogenic viscerotropic Newcastle disease (VVND). Exotic Newcastle disease (END) consists of both VVND and VNND. The Newcastle disease virus itself (NDV) is also called avian paramyxovirus-1 or APMV-1. Newcastle disease is peste avícola de Egipto in Spanish, Newcastle-Krankheit in German, hoensepest in Danish, and ayam tetélo in Indonesian.

Description As of 2009, Newcastle disease is the most important poultry disease (and perhaps the one with the most acronyms). It is endemic in the Middle East, Africa, and Central and South America, but outbreaks occur worldwide. The agent is a paramyxovirus, like the agents of measles and rinderpest. ND has four forms, or pathotypes: • Asymptomatic enteric: birds do not appear sick. • Lentogenic: birds have mild respiratory illness. • Mesogenic: birds have major respiratory or neurological symptoms, with mortality up to about 10 percent. • Velogenic: either neurotropic, with respiratory or neurological symptoms (VNND), or viscerotropic, with hemorrhagic lesions in the intestine (VVND); mortality may exceed 90 percent. “Virulent” ND includes the mesogenic, VNND, and VVND pathotypes, but “exotic” ND means VNND or VVND. In some virulent ND outbreaks, 100 percent of birds in a flock show symptoms, and 90 percent die within days after exposure. All forms spread mainly by aerosol transmission or direct contact with other birds or infected surfaces. Outbreaks often result from illegal importation of birds for the pet trade or cockfighting. Pigeons that scavenge feed from poultry operations may spread the disease. NDV can also cause illness in humans. Most of these infections are mild, but there is one report of fatal NDV pneumonia after peripheral blood stem cell transplant surgery. Humans can also act as carriers and transmit the virus to other people or birds. Many other animal species



serve as hosts or mechanical vectors. The virus remains active in moist soil for 22 days, on feathers at room temperature for 123 days, and in lake water for 19 days. Which Animals Are at Risk? Chickens, pigeons, ducks, parrots, and many wild migratory birds are at risk for ND, even after vaccination. Chickens are highly susceptible, but some birds, including turkeys and budgies, may harbor the infection without showing obvious signs. Virulent strains are endemic in wild cormorants, and there is concern that gulls might transfer the disease between cormorant colonies and farms. ND poses no serious risk to most humans, but poultry workers sometimes develop malaise or eye irritation. The Numbers A 1971–1973 outbreak caused the deaths of about 12 million chickens in southern California, with estimated losses of $56 million. Some chickens died of the disease itself, whereas others were killed to stop the outbreak. An outbreak in Italy in 1999–2000 necessitated the culling of 13 million chickens and guinea fowl. In 2000, an outbreak in Mexico destroyed nearly 14 million chickens. The most recent U.S. outbreak, in 2003, cost $160 million and claimed the lives of 4 million chickens in southern California, Arizona, and Nevada. History The first ND outbreak in the British Isles took place at Newcastle-upon-Tyne in 1927, the year after the disease made its global debut in Indonesia. In 1956, however, researchers found records of a similar disease that killed all the chickens in the Western Isles of Scotland in 1896. Surviving farmers remembered that the sick chickens wheezed and staggered. But since other bird diseases (such as avian influenza) can cause similar symptoms and high mortality, the 1896 outbreak may never be positively identified. Virulent forms of ND reached the United States in about 1945, possibly with infected partridges and pheasants imported from Hong Kong. Major outbreaks occurred in southern California in 1971 and 2002. As of 2009, the United States has been free of Newcastle disease outbreaks since 2003. Several recent sources claim that Newcastle disease drove the North American passenger pigeon (Ectopistes migratorius) to extinction. But the last wild passenger pigeons died in 1899, and the last known passenger pigeon died in a zoo in 1914, long before there was any evidence of Newcastle disease in North America. ND was not even discovered until 1926, and the Scottish outbreak of 1896 (whatever it was) did not affect New World poultry. Thus, the claim is dubious at best. The source most often cited is IUCN 2008, which cites BirdLife International, which cites several review papers—which simply mention Newcastle disease as one of several factors that might have contributed to the extinction of the passenger pigeon. More likely factors include hunting, deforestation, and an unrelated parasitic disease called trichomoniasis. Prevention and Treatment ND is controllable, but the global cost of vaccination, surveillance, and testing may exceed that of any other animal disease. Commercial vaccines for some strains have been available since



1944, and vaccination is routine in some countries (Case Study 4-8). Methods include spraying entire flocks, adding vaccines to feed or water, or Many rural villages in the tropics have no vaccinating individual birds (Figure 4.9). refrigeration facilities for transport and The live ND vaccine is effective, but it is storage of vaccines. In 2005–2007, three unpopular because of its potential ability to agricultural organizations in Tanzania revert to full virulence. Since 1970, inactivated collaborated on a project to increase rural poultry productivity by making a heatvaccines have also been available. In 2006, stable Newcastle disease vaccine available researchers in Mexico reported the invention of to farmers and teaching them how to use it. genetically modified maize that induces ND antiBy the end of 2006, the vaccination probody production when fed to poultry. gram had decreased chicken mortality by If chicks are not vaccinated during the first 80 percent. Average household poultry profour days of life, vaccination should be postduction increased from 16 to 74 chickens, poned until the third week to avoid maternal antiwith concomitant improvement in family body interference with active immune response. nutrition and financial security. Many parSome countries prohibit ND vaccination because ticipants invested their surplus income in of the problem of distinguishing between other livestock or facilities. infected and vaccinated flocks. Other control measures include quarantine and disinfection of contaminated areas. Heat, bleach, or ultraviolent light deactivates the virus on environmental surfaces. Case Study 4-8: Taking the Heat

Figure 4.9 A baby chick receives a virosome vaccine to protect it from exotic Newcastle disease. Source: U.S. Department of Agriculture, Agricultural Research Service.



Popular Culture In 1962, Cuban Premier Fidel Castro claimed that the United States had deliberately infected his country’s flocks with Newcastle disease. A Canadian poultry expert who visited Cuba reportedly told the press that the U.S. Central Intelligence Agency (CIA) had paid him $5,000 to introduce ND to Cuban turkeys. This expert further claimed that he discarded the viral cultures after accepting the money and never carried out his mission, yet an outbreak occurred in Cuba soon after his visit. ND is highly infectious, and the true source of the 1962 outbreak is unknown. It is illegal to import cascarones—confetti-filled eggshells used in Easter celebrations— from Mexico to the United States because of the danger of spreading Newcastle disease to poultry. Goosey Fair was an annual event in the town of Tavistock in southern England for over 800 years, where people bought their Christmas geese at an open market. After the mid-1960s, however, laws enacted to limit the spread of Newcastle disease made it illegal to sell live poultry at markets. According to a field manual, African folk cures for ND include any of the following added to water: white vinegar, ground chili peppers, mango or tamarind bark, detergent, potassium permanganate, ground garlic, cactus sap, or car battery acid. Some African farmers associate outbreaks with the Harmattan (a seasonal dry wind), whereas others believe the disease strikes at Christmas time, or when mango trees are flowering—or when diseased birds are nearby. Popular control measures include selling sick birds, or eating them as quickly as possible and burying the leftovers.

The Future Since about 1964, doctors have administered vaccine strains of Newcastle disease virus to human cancer patients as an oncolytic (tumor-destroying) agent or immune enhancer. Some clinical trials with NDV have yielded positive results, but the results are controversial. As of 2009, research in this area is continuing.

References and Recommended Reading Aldous, E. W., and D. J. Alexander. “Newcastle Disease in Pheasants (Phasianus colchicus): A Review.” Veterinary Journal, Vol. 175, 2008, pp. 181–185. Alexander, D. J., et al. “Characterization of Paramyxoviruses Isolated from Penguins in Antarctica and SubAntarctica During 1976–1979.” Archives of Virology, Vol. 109, 1989, pp. 135–143. Alexander, D. J. “Newcastle Disease and Other Avian Paramyxoviruses.” Revue Scientifique et Technique, Vol. 19, 2000, pp. 443–462. Blockstein, D. E., and H. B. Tordoff. “Gone Forever: A Contemporary Look at the Extinction of the Passenger Pigeon.” American Birds, Vol. 39, 1985, pp. 845–851. Broder, J. M. “8,000 California Birds Killed in Bid to Stop Virus.” New York Times, 26 October 2002. Chakrabarti, S., et al. “Detection and Isolation of Exotic Newcastle Disease Virus from Field-Collected Flies.” Journal of Medical Entomology, Vol. 44, 2007, pp. 840–844. El Saawi, N. “Crying Fowl Play.” Associated Press, 23 February 2003. “Exotic Newcastle Disease.” Factsheet, USDA Animal and Plant Health Inspection Service (APHIS) Veterinary Services, January 2003. Goebel, S. J., et al. “Isolation of Avian Paramyxovirus 2 from a Patient with a Lethal Case of Pneumonia.” Journal of Virology, Vol. 81, 2007, pp. 12709–12714.



Guerrero-Andrade, O., et al. “Expression of the Newcastle Disease Virus Fusion Protein in Transgenic Maize and Immunological Studies.” Transgenic Research, Vol. 15, 2006, pp. 455–463. Hanson, R. P. “The Possible Role of Infectious Agents in the Extinctions of Species.” Pages 439–454 in Hickey, J. J. (Ed.). 1969. Peregrine Falcon Populations. Madison: University of Wisconsin Press. Huang, Z., et al. “Recombinant Newcastle Disease Virus as a Vaccine Vector.” Poultry Science, Vol. 82, 2003, pp. 899–906. “Illegal Bird Smuggling Could Cause Disease.” United Press International, 8 January 2005. MacPherson, L. W. “Some Observations on the Epizootiology of Newcastle Disease.” Canadian Journal of Comparative Medicine, Vol. 20, 1956, pp. 155–168. Maendeleo Agricultural Technology Fund. “Dissemination of Thermo-Stable New Castle Disease Vaccine in Rural Chickens of Mwanza Region, Tanzania.” MATF Newsletter, Vol. 6, 2007, pp. 14–15. Romero, S. “Virus Takes a Toll on Texas Poultry Business.” New York Times, 16 May 2003. Sawahel, W. “GM Maize Protects Chickens from Deadly Virus.” Science and Development Network, 18 August 2006. Schorger, A. W. 1955. The Passenger Pigeon: Its Natural History and Extinction. Madison: University of Wisconsin Press. Senne, D. A., et al. “Control of Newcastle Disease by Vaccination.” Developments in Biologicals (Basel), Vol. 119, 2004, pp. 165–170. Sinkovics, J. G., and J. C. Horvath. “Newcastle Disease Virus (NDV): Brief History of Its Oncolytic Strains.” Journal of Clinical Virology, Vol. 16, 2000, pp. 1–15. Spradbrow, P. B. “Epidemiology of Newcastle Disease and the Economics of Its Control.” Workshop Proceedings, Danish Agricultural and Rural Development Advisers’ Forum, 1999. Verwoerd, D. J. “Ostrich Diseases.” Revue Scientifique et Technique, Vol. 19, 2000, pp. 638–661. Zulkifli, M. M., et al. “Newcastle Diseases Virus Strain V4UPM Displayed Oncolytic Ability against Experimental Human Malignant Glioma.” Neurological Research, 18 October 2008.

AVIAN INFLUENZA Summary of Threat Avian influenza or bird flu is the same disease as influenza A (Chapter 2), but most strains that infect birds appear harmless to humans and vice versa. Some bird flu strains, including the highly publicized H5N1, can cause severe illness in both birds and humans and might have the potential to cause deadly pandemics. Avian influenza is classified as a biosecurity threat under the Bioterrorism Protection Act of 2002.

Other Names The names of influenza A antigenic subtypes refer to glycoproteins on the surface of the virus (see Figure 2-7, page 33). The letter H followed by a number identifies a glycoprotein called a hemagglutinin, and N followed by a number identifies another glycoprotein called a neuraminidase. Thus, H5N1 is the influenza A virus subtype that has hemagglutinin 5 and neuraminidase 1. Within each subtype are various strains, some more dangerous than others. Some strains or subtypes also have common names based on the animal species they usually infect, such as avian (bird) flu, equine (horse) flu, canine (dog) flu, and porcine (swine) flu. The acronym HPAI stands for “highly pathogenic avian influenza.” (In this case, the H does not stand for hemagglutinin.) HPAI was once called fowl plague, a name that now usually refers to Newcastle disease. Less dangerous strains are called LPAI (low pathogenic avian influenza) or



NPAI (non-pathogenic avian influenza). Words for influenza in most languages refer to the human disease (Chapter 2). Description Whether the patient is a bird, a human, or a horse, the avian influenza virus (Figure 4.10) causes high fever, breathing difficulty, nasal discharge, and the appearance of discomfort. In birds, egg production may drop and feathers may appear ruffled. Although most strains are relatively harmless, HPAI is an exception. It often causes additional symptoms, such as swelling, greenish diarrhea, hemorrhaging under the skin, and neurological complications. HPAI can rapidly kill large numbers of birds. Poultry workers and other exposed humans can also contract bird flu, and in a few cases it has spread directly from one human to another. In 2006, a person in Indonesia transmitted H5N1

Figure 4.10 Transmission electron micrograph showing avian influenza virus H5N1. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.



to six household members, and one infected an eighth person. But bird flu remains largely a disease of birds, and the feared human pandemic has not yet happened. As of 2009, avian influenza occurs worldwide, but the strains known as HPAI (H5N1 and others) have not been reported in the United States since 2004. Transmission of avian influenza is usually by close-range airborne inhalation, direct contact with infected animals, ingestion of infected birds, or contact with contaminated surfaces. The incubation period ranges from a few days to one week. Which Animals Are at Risk? Domestic chickens, turkeys, geese, parrots, ostriches, and other birds are at risk for avian influenza. It spreads rapidly and causes high mortality in confined poultry feeding operations, but migratory wild ducks, gulls, and shorebirds sometimes carry the virus in their intestines without becoming sick. Humans have contracted bird flu by prolonged contact with infected poultry (or people), but apparently not by handling, cooking, or consumption of dressed poultry meat. Sewer workers exposed to contaminated material may also be at risk. Domestic dogs, cats, and other animals that eat infected birds may contract the disease (Case Study 4-9). Alligators and crocodiles are also potential hosts, but studies have been inconclusive. The Numbers H5N1 has killed hundreds of millions of birds in Russia, the Middle East, Europe, and Africa, but it is not the only potentially lethal subtype. The 1983 outbreak of H5N2 in the northeastern United States killed an estimated 17 million chickens. As of 2008, there were 16 known hemagglutinin (H) subtypes and 9 known neuraminidase (N) subtypes, for a total of 144 (16 ⫻ 9) possible influenza subtypes, all with possibly different host susceptibilities. History Case Study 4-9: Tweety Nails Sylvester In 2004, the media reported that HPAIH5N1 avian influenza killed a large number of tigers at two zoological parks in Thailand. In both cases, the tigers apparently contracted the disease by eating raw or inadequately cooked chicken or pork. One zoo had 441 tigers, of which 45 died of influenza and 102 were euthanized. Antiviral drugs may have saved some of them. At the other zoo, two tigers and two leopards died of the same disease. The tiger is an endangered species, and the 149 tigers that died of bird flu represented about 3 percent of all tigers in the world.

Avian influenza has existed for centuries (or longer), but the first known cases of subtype H5N1 were in Scotland in 1959. It reportedly killed two flocks of chickens, but it was not the same as the highly pathogenic H5N1 virus that arose in China in 1997 and resurfaced in 2004. The subtype alone does not determine pathogenicity; each subtype has various strains. Table 4.2 summarizes the most common subtypes with the dates and locations of recent outbreaks. Prevention and Treatment Influenza vaccines can control losses by reducing viral replication and shedding. In the



Table 4.2 Recent Avian Influenza Outbreaks Subtype H5N1 H5N2 H5N2 H5N2 H5N2 H7N1 H7N3 H7N3 H7N4 H7N7

Outbreak 1997 1983 1994 1997 2004 1999 1994 2002 1997 2003

Location Europe, Asia, Africa Pennsylvania Mexico Italy Texas Italy Australia, Pakistan Chile Australia Netherlands

United States, the use of H5 and H7 avian influenza vaccines on animals requires USDA approval. In 2008, U.S. researchers reported a new vaccine that could protect chickens, cats, and humans in the event of a bird flu pandemic. Infected flocks can also be treated with antibiotics to control secondary infections. In 2006, the FDA prohibited the use of antiviral drugs to treat poultry because of the danger of drug resistance. As of 2009, there is no proof that humans have caught avian influenza by handling dressed poultry, but reasonable precautions are in order. Eating raw chicken (or feeding it to the dog, cat, or pig) is clearly out. Consumers should cook poultry thoroughly and wash anything that comes in contact with raw poultry or eggs.

Popular Culture The 2006 made-for-TV movie Fatal Contact: Bird Flu in America is not a documentary but a work of fiction, in which the H5N1 influenza virus mutates into a pandemic form that spreads easily from person to person. An American businessman visiting China contracts the virus in a Hong Kong market and takes it home. The movie highlights the importance of cooperation and planning, and even mentions Tamiflu® resistance. As expected, the pandemic swamps the healthcare system and disrupts other public services. During the 2004 avian influenza outbreak, investigators tracked rumors of outbreaks in both humans and animals. Most rumors appeared within the first seven weeks after the public health alert; even in a crisis, people quickly adjust and go on with their lives. Rumors regarding human cases were both more numerous and less likely to be true than those regarding animal outbreaks. The findings were consistent with the basic law of rumor, which states that the number of rumors in circulation is roughly equal to the importance of the rumor times the uncertainty surrounding the rumor. As more information becomes available, uncertainty decreases, and fewer rumors circulate even if the importance remains high. In 2005, the media reported that British scientists quarantined a parrot imported from Surinam that was suspected of having avian influenza. Eventually, someone noticed that the parrot was already dead.



The Future For years, some scientists have warned that H5N1 or a related virus could mutate to a form resembling the Spanish Flu on steroids and wipe out as many as 1 billion people. Others, however, have concluded that the high death rate in the 1918 pandemic resulted mainly from secondary bacterial infections and not from unique properties of the flu itself. Thus, to mix a metaphor, bird flu (like the 2009 swine flu) may be a paper tiger. The real problem that won’t go away might be antibiotic resistance (Chapter 3), which could make it nearly as hard to fight bacterial infections in 2018 as in 1918.

References and Recommended Reading Alexander, D. J. “An Overview of the Epidemiology of Avian Influenza.” Vaccine, Vol. 25, 2005, pp. 5637–5644. Causey, D., and S. V. Edwards. “Ecology of Avian Influenza in Birds.” Journal of Infectious Disease, Vol. 197, Supplement 1, 2008, pp. S29–S33. Davis, L. M., and E. Spackman. “Do Crocodilians Get the Flu? Looking for Influenza A in Captive Crocodilians.” Journal of Experimental Zoology, Part A, Ecological Genetics and Physiology, 31 March 2008. Fish, D. “What About the Ducks? An Alternative Vaccination Strategy.” Yale Journal of Biology and Medicine, Vol. 78, 2005, pp. 301–308. Fitzpatrick, S. “Jakarta Bird Flu Theory ‘Nutty.’” The Australian, 27 February 2008. Gharaibeh, S. “Pathogenicity of an Avian Influenza Virus Serotype H9N2 in Chickens.” Avian Diseases, Vol. 51, 2008, pp. 106–110. Gilbert, M. “Climate Change and Avian Influenza.” Revue Scientifique et Technique, Vol. 27, 2008, pp. 459–466. Lipatev, A. S., et al. “Domestic Pigs have Low Susceptibility to H5N1 Highly Pathogenic Avian Influenza Viruses.” PLoS Pathogens, Vol. 4, 2008, pp. e1000102. Londt, B. Z., et al. “Highly Pathogenic Avian Influenza Viruses with Low Virulence for Chickens in In Vivo Tests.” Avian Pathology, Vol. 36, 2007, pp. 347–350. Marangon, S., and L. Busani. “The Use of Vaccination in Poultry Production.” Revue Scientifique et Technique, Vol. 26, 2007, pp. 265–274. McDowell, R. “US Controls Bird Flu Vaccines over Bioweapon Fears.” Associated Press, 11 October 2008. Mumford, E. L., and U. Kihm. “Integrated Risk Reduction along the Food Chain.” Annals of the New York Academy of Sciences, Vol. 1081, 2006, pp. 147–152. Mumford, E. L., et al. 2007. “Avian Influenza H5N1: Risks at the Human-Animal Interface.” Food and Nutrition Bulletin, Vol. 28 (Supplement), 2007, pp. S357–S363. Olsen, B., et al. “Global Patterns of Influenza A Virus in Wild Birds.” Science, Vol. 312, 2006, pp. 384–388. Rosenthal, E. “Bird Flu Reports Multiply in Turkey, Faster than Expected.” New York Times, 9 January 2006. Samaan, G., et al. “Rumor Surveillance and Avian Influenza H5N1.” Emerging Infectious Diseases, Vol. 11, 2005, pp. 463–466. Sims, L. D., et al. “Origin and Evolution of Highly Pathogenic H5N1 Avian Influenza in Asia.” Veterinary Record, Vol. 157, 2005, pp. 159–164. Song, D., et al. “Transmission of Avian Influenza Virus (H3N2) to Dogs.” Emerging Infectious Diseases, Vol. 14, 2008, pp. 741–746. Spackman, E. “A Brief Introduction to the Avian Influenza Virus.” Methods in Molecular Biology, Vol. 436, 2008, pp. 1–6. Specter, M. “Nature’s Bioterrorist.” The New Yorker, 5 February 2005. Srikantiah, S. “Mass Culling for Avian Influenza: Rational Strategy or Needless Destruction?” Indian Journal of Medical Ethics, Vol. 5, 2008, pp. 52–54. Thanawongnuwech, R., et al. “Probable Tiger-to-Tiger Transmission of Avian Influenza H5N1.” Emerging Infectious Diseases, Vol. 11, 2005, pp. 699–701.



“Vaccine Protects Against Bird Flu.” United Press International, 20 October 2008. Walsh, B. “Living Cheek by Beak in Indonesia.” Time, 14 June 2007. Weber, T. P., and N. I. Stilianakis. “Ecologic Immunology of Avian Influenza (H5N1) in Migratory Birds.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1139–1143. Yamada, T., et al. “Ready for Avian Flu?” Nature, Vol. 454, 2008, p. 162. Zamiska, N. “How Academic Flap Hurt World Effort on Chinese Bird Flu.” Wall Street Journal, 27 February 2006.

HONEYBEE COLONY COLLAPSE DISORDER Summary of Threat In colony collapse disorder, large numbers of bees die or fail to return to the hive. As of 2009, scientists have not yet determined the exact reason for this phenomenon. Parasites, bacteria, viruses, fungi, stress, and pesticides all may be contributing factors. There is evidence that periodic die-offs of bee colonies have plagued humanity for thousands of years.

Other Names Colony collapse disorder is also called CCD, BCCD (bee colony collapse disorder), fall dwindle, spring dwindle, May disease, autumn collapse, bee die-off, hive death, disappearing disease, vanishing bee syndrome, or Mary Celeste syndrome. Most of these names are selfexplanatory; the last refers to a ship that was found sailing the Atlantic in 1872 without its passengers or crew. One website author facetiously identifies colony collapse disorder as a psychiatric problem called ADHBee, with reference to the contemporary buzzword—sorry, now we’re doing it— ADHD, or attention deficit hyperactivity disorder. In other words, the bees lose interest in the things we want them to do (visiting flowers or making wax or whatever) and just wander off. Facetious or not, it’s as good an explanation as any to date.

Description As of 2009, colony collapse disorder is a symptom rather than a disease in the usual sense. Worker bees (Figure 4.11) fail to return to the hive, and the colony dies, but experts are not sure why. There is some evidence that such die-offs are simply a characteristic of honeybee colonies, and that the crisis is largely an illusion. Various studies have identified the culprit as Israeli acute paralysis virus, deformed wing virus, an Asian bee parasite (Nosema ceranae), or the familiar varroa mites (Figure 4.12) and tracheal mites that decimated American bee colonies in the mid-1980s. Other studies have implicated clothianidin and other pesticides, electromagnetic radiation from cell phones, inbreeding, climate change, habitat loss, immune suppression, or stress (Case Study 4-10). But while some farmers complain about a shortage of bees, others claim that there are too many bees in the wrong places. For example, almond growers in California’s San Joaquin Valley need bees for pollination, but tangerine growers on adjacent farms need to keep bees away. If pollinated, tangerines develop unwanted seeds (pips) that reduce their market value. Similar problems affect seedless grapes and watermelons. The law protects bees by requiring growers to avoid



Figure 4.11 Honeybee worker, drone, and queen. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

Figure 4.12 Varroa jacobsoni, a mite that lives as a parasite on honeybees. Source: U.S. Department of Agriculture, Agricultural Research Service.


spraying for pests when bees are present, but scheduling conflicts are inevitable.

Which Animals (and Plants) Are at Risk? Bees extract nectar from flowers, modify it by digestion and evaporation, and store it in the form that we call honey. But in the process of gathering nectar, the bees also collect pollen on their bodies and transfer it to other flowers, more efficiently than wind alone could do. This is the plant world’s equivalent of sex. Thus, anything that threatens bees also threatens many plants (Table 4.3). Colony collapse disorder has affected managed honeybee colonies in North America, Europe, and Asia at least since 2006. Most wild bee species are not at risk for colony collapse because they do not live in colonies, but they might be individually susceptible to whatever disease, pesticide, or other stressors may be causing colony collapse. As of 2009, the cause and risk factors remain unknown.


Case Study 4-10: Give Bees a Chance Stress is more than a human malady. To the extent that the term encompasses a range of biological responses to perceived threats or unfavorable conditions, it is probably fair to say that bees can experience stress. The question is whether a commercial bee lot subjects bees to a level of stress for which evolution has not prepared them. Wild honeybees usually build three or four hives per square mile, for example, whereas managed colonies are packed together in rows a few feet apart. When forage is scarce, farmers keep bees alive by giving them highfructose corn syrup. And wild honeybees normally have a winter rest period, but winter-blooming crops won’t wait. In 2007, journalists described how beekeepers from all over the United States converged on California in a mad dash to pollinate the almond crop and collect their money before the bees dropped dead. Perhaps the majority of bees simply cannot adjust to fast food and a commuter lifestyle.

Table 4.3 Food Crops That Require Bees for Pollination Name



Almond Apple Apricot Avocado Blackberry Blueberry Brazil nut Broccoli Brussels sprouts Buckwheat Cabbage Cacao Canola Cantaloupe Casaba melon Cashew Cauliflower Chayote Cherry Citron

Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, stingless bees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Bumblebees, orchid bees, carpenter bees Honeybees, solitary bees Honeybees, solitary bees Honeybees, solitary bees Honeybees, solitary bees Flies and unidentified wild bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, stingless & solitary bees Honeybees, solitary bees Honeybees, stingless bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees

Nut Fruit Fruit Fruit Fruit Fruit Nut Flower, stem Leaves Seed Leaves Seed (cocoa) Seed, oil Fruit Fruit Nut Flower Fruit Fruit Fruit (Continued)



Table 4.3 (Continued) Name



Cranberry Crenshaw melon Cucumber Currant Dewberry Eggplant Feijoa Fennel Gooseberry Hazelnut Honeydew melon Huckleberry Jujube Kiwi fruit Kohlrabi Loquat Macadamia Mango Mustard Nectarine Onion Parsley Parsnip Passionfruit Peach Pear Persian melon Persimmon Plum Pumpkin Radish Raspberry Rutabaga Squash Starfruit Sunflower Tea Turnip Watermelon

Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, solitary bees Honeybees, solitary bees Honeybees, solitary bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, solitary bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, solitary bees Honeybees, bumblebees Honeybees, stingless bees, solitary bees Honeybees, stingless bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, solitary bees Honeybees, flies Honeybees, solitary bees Carpenter bees, solitary bees, bumblebees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees Honeybees, stingless bees Honeybees, wild bees Wild bees Honeybees, solitary bees Honeybees, bumblebees, solitary bees

Fruit Fruit Fruit Fruit Fruit Fruit Fruit Seed, bulb Fruit Nut Fruit Fruit Fruit Fruit Leaves Fruit Nut Fruit Seed, oil Fruit Bulb Leaves Root Fruit Fruit Fruit Fruit Fruit Fruit Fruit Root Fruit Root Fruit Fruit Seed, oil Leaves Root, leaves Fruit

Note: Many other crops also benefit from bee pollination but do not absolutely require it. Sources differ as to the primary pollinators for certain plants. Source: USDA Agricultural Research Service.

The Numbers In the United States, an estimated 2.4 million to 3 million managed honeybee colonies pollinate $14 billion worth of crops every year. In addition to the value of the crops themselves, beekeepers earn a living by supplying farmers with beehives for pollination. In 2005, beekeepers in California alone received over $121 million for this service, in addition to sales of 10,000 tons of honey and 200 tons of beeswax.



History In the fall of 2006, American beekeepers reported that approximately one-third of all managed colonies were suddenly vacant for no apparent reason. By the end of 2007, the problem was worse; according to a report in Science, between 50 percent and 90 percent of all honeybee colonies in the United States were lost. Bee diseases and pests may spread more rapidly nowadays because of the frequent long-distance transport of beehives, but the myth of Aristaeus (see Popular Culture) suggests that beekeepers have had similar problems for thousands of years. When colonists brought the honeybee to America in the 1600s, its diseases and pests came along for the ride. Beekeepers reported large die-offs in the 1890s, and something called “disappearing disease” affected many colonies in the late 1970s. Honeybees, like all living things, coexist with a host of microbes, parasites, predators, and competitors whose precise interactions may never be fully understood, although the effort continues. Prevention and Treatment Agricultural extension offices distribute literature on methods of protecting bees from pesticides and other known or suspected stressors. There are also online and traditional college courses in beekeeping management. Unfortunately, no one knows exactly how to prevent colony collapse disorder. Chemical pesticides are available for treatment of mite infestations, but some of these chemicals also harm bees, and others have become less effective on mites due to resistance. Popular Culture Archaeological evidence shows that people in Egypt and the Middle East have raised honeybees in portable hives for at least 5,000 years. According to ancient Greek mythology, the first beekeeper was Aristaeus, who also dabbled in the nascent olive oil and cheesemaking industries. He was doing quite well, until one day he chased after a married woman—the wife of the divine Orpheus, worse luck—and she stepped on a venomous snake and died. Thus, the gods punished Aristaeus by killing all his bees. Olives are wind-pollinated, but honey and wax were also valuable commodities, and Aristaeus was devastated. But instead of apologizing to the widower, or trying to figure out what went wrong, Aristaeus scolded his mother for not protecting him. (The story is reminiscent of many a dispute between the farming industry and the USDA.) Eventually, on the advice of a shape-shifting prophet, Aristaeus made amends by sacrificing some cattle in a sacred grove. Nine days later, he returned to the grove and found that a swarm of wild bees had landed on one of the carcasses, thus putting him back in business. In ancient times, many European societies regarded bees as messengers who notified the gods when a person died. This tradition may explain the rural European and American custom of “telling the bees” about the death of a household member. If not thus informed, the bees may die or stop making honey. Other popular beliefs held that bees would die if purchased on a Friday, or if purchased for cash instead of barter, or if people quarreled about their ownership. In A.D. 77, Pliny the Elder wrote that a swarm of bees would die if a menstruating woman looked at them. These beliefs suggest that bee colonies have always tended to die unexpectedly. The Future Honeybee colonies will probably continue to suffer massive die-offs, because they have always done so. One possible solution is to encourage more pollination of crops by wild native



bees. Many wild bees nest in the ground, for example, so farmers need to watch where they plow. These insects are also vulnerable to pesticides, and they need flowers during the breeding season. But with a bit of effort and planning, some farms near native habitats can receive full pollination from wild bees alone.

References and Recommended Reading Aliouane, Y., et al. “Subchronic Exposure of Honeybees to Sublethal Doses of Pesticides: Effects on Behavior.” Environmental Toxicology and Chemistry, 13 August 2008. Amdam, G. V., and S.-C. Seehuu. “Order, Disorder, Death: Lessons from a Superorganism.” Advances in Cancer Research, Vol. 95, 2006, pp. 31–60. Anderson, D., and I. J. East. “The Latest Buzz about Colony Collapse Disorder.” Science, Vol. 319, 2008, pp. 724–725. Antúnez, K., et al. “Honeybee Viruses in Uruguay.” Journal of Invertebrate Pathology, Vol. 93, 2006, pp. 67–70. Ariana, A., et al. “Laboratory Analysis of Some Plant Essences to Control Varroa destructor (Acari: Varroidae).” Experimental and Applied Acarology, Vol. 27, 2002, pp. 319–327. Barbassa, J. “Honeybee Deaths Increase.” Associated Press, 7 May 2008. Benjamin, A. “Last Flight of the Honeybee?” The Guardian, 31 May 2008. “Clues Sought in Honey Bees’ Demise.” United Press International, 1 July 2008. Cone, T. “Tangerine Growers Tell Beekeepers to Buzz Off.” Associated Press, 9 January 2009. Cox-Foster, D. L., et al. “A Metagenomic Survey of Microbes in Honey Bee Colony Collapse Disorder.” Science, Vol. 318, 2007, pp. 283–287. Delaplane, K. S., and D. F. Mayer. 2000. Crop Pollination by Bees. New York: CABI Publishing. Farley, J.D. “Bee by Bee.” New York Times, 30 June 2008. “ Honeybee Disorder Still Stumps Researchers.” United Press International, 5 January 2009. Kay, J. “Lawsuit Seeks EPA Pesticide Data.” San Francisco Chronicle, 18 August 2008. Kuchinskas, S. “Are the Bees Dying Off Because They’re Too Busy?” East Bay Express, 11 August 2007. Muz, M. N. “Sudden Die-Off of Honeybee Colonies.” Türkiye Parazitolojii Dergisi, Vol. 32, 2008, pp. 271–275. [Turkish] Pinto, M. A., et al. “Temporal Pattern of Africanization in a Feral Honeybee Population from Texas Inferred from Mitochondrial DNA.” Evolution, Vol. 58, 2004, pp. 1047–1055. Revkin, A. C. “Bees Dying: Is It a Crisis or a Phase?” New York Times, 17 July 2007. Roulston, T. H. “Practices That Encourage Native Bees in Vine Crops.” Great Lakes Fruit Vegetable and Farm Market Expo, Grand Rapids, MI, 9–11 December 2008. Russell, S. “UCSF Scientist Tracks Down Suspect in Honeybee Deaths.” San Francisco Chronicle, 26 April 2007. Seeley, T. D., and D. R. Tarpy. “Queen Promiscuity Lowers Disease Within Honeybee Colonies.” Proceedings Biological Sciences, Vol. 274, 2007, pp. 67–72. Shen, M., et al. “Intricate Transmission Routes and Interactions between Picorna-like Viruses (Kashmir Bee Virus and Sacbrood Virus) with the Honeybee Host and the Parasitic Varroa Mite.” Journal of General Virology, Vol. 86, 2005, pp. 2281–2289.

CONCLUSION Infectious disease outbreaks represent a major threat for species that live in densely packed communities. This statement applies to wild bee colonies, bat caves, and human cities, as well as cattle feedlots and crowded piggeries. New vaccines and genetically modified livestock strains may alleviate this problem, but new diseases will continue to appear. Populations that pass through a bottleneck of disease will theoretically emerge with enhanced resistance, but that reward offers small consolation in the short term.


Food Insecurity, Continued

The great peril of our existence lies in the fact that our diet consists entirely of souls. —Attributed to Aua, Inuit shaman

A major die-off of livestock might plunge world markets into chaos and exacerbate international tensions, but global famine would not be automatic. Meat and milk represent only about 9 percent of total caloric intake in low-income nations and 24 percent in high-income nations. The balance of the human diet consists of grains and other plant products. Nor is this a modern aberration; many hunter-gatherer societies obtained an estimated 15 percent of their diet from animals and 85 percent from plants. In other words, plants are what we really need. If even one staple crop fails, such as rice, wheat, or maize, widespread starvation may result. Rice alone represents about 20 percent of the world’s food, and wheat and maize together account for another 40 percent. So how safe are these resources? Table 5.1 lists examples of past outbreaks, and Table 5.2 summarizes major diseases of staple crops. Before dismissing the ten examples in this chapter as inconsequential brown spots or green bugs, consider the fact that the U.S. Department of Homeland Security lists some of them as biosecurity threats. These tiny adversaries (and hundreds of others) have caused more death and economic devastation than any human army, and in many cases we don’t know how to stop them.

CITRUS TRISTEZA VIRUS Summary of Threat Citrus tristeza virus (CTV) is a catastrophic disease of orange, grapefruit, and other citrus fruits, which are among the most important cash crops in tropical and subtropical regions worldwide. Transmission is mainly by aphid vector, grafting, and mechanical damage. Outbreaks have destroyed millions of trees and caused great economic damage. Control of tristeza is difficult, and new strains continue to arise.



Table 5.1 Some Major Outbreaks of Plant Diseases and Pests Disease



Estimated Losses

Citrus tristeza virus Citrus tristeza virus Citrus tristeza virus Bacterial wilt (tomato) Bacterial wilt (banana) Southern corn leaf blight Citrus canker Late blight of potato Late blight of potato Soybean rust Witches’ broom disease Phoma stem canker Wheat rust Asian soybean aphid Desert locust

1940s 1984–1986 2002 1966–1968 2006 1970 1984–1989 1845–1849 1997 2003 1989 2004 1954 2000–2002 2004

Brazil Florida Italy Philippines Uganda United States Florida Ireland Peru Brazil Brazil Argentina United States United States West Africa

9 million citrus trees 50% of citrus crop 10,000 citrus trees 15% of tomato crop Up to 90% of banana crop 15% of corn crop 20 million citrus trees1 Potato crop + 1 million humans 80% of potato crop $1.3 billion 90% of cacao crop 32% of canola in affected fields 40% of wheat crop $2.2 billion $2.5 billion


Burned as part of an unsuccessful campaign to eradicate the disease.

Other Names Citrus tristeza virus is also called CTV, citrus tristeza closterovirus, citrus quick decline virus, tristeza-quick decline (T-QD) virus, grapevine A virus, grapefruit stem pitting virus, grapefruit stunt bush virus, Ellendale mandarin decline virus, hassaku dwarf virus, citrus seedling yellows virus, and lime dieback virus. Names in other languages include tristeza dos citros (Portuguese, “sadness of citrus”) and podredumbre de las raicillas (Spanish, “corruption of citrus”).

Description The agent is an RNA virus that infects citrus trees, causing loss or discoloration of foliage or stem pitting (Figure 5.1). Infected trees may die within a few months or survive for years in poor condition, producing small fruit. This disease may occur wherever citrus trees are present. Specific effects depend on scion varieties and rootstock combinations, but there are three distinct syndromes: • Tristeza, the “quick decline” form of the disease, first seen on citrus grafted on sour orange, with wilting and dieback • Stem pitting or honeycombing, visible under the bark on small branches • Seedling yellows, with stunting, curling, and yellowing of leaves The most efficient vectors for this disease are brown citrus aphids (Toxoptera citricida, Case Study 5-1), but other aphids get the job done. Trees also become infected by grafting and mechanical inoculation, or by way of a parasitic plant called a bridging dodder.

Table 5.2 The World’s Staple Crops and Their Principal Diseases Crop






Mildew (Erysiphe graminis) Spot blotch (Cochliobolus sativus) Scald (Rhynchosporium secalis) Scab (Gibberella zeae) Rusts (Puccinia) Net blotch (Pyrenophora teres) Barley stripe (Pyrenophora graminea) Smuts (Ustilago)

Barley yellow dwarf luteovirus Barley stripe mosaic hordeivirus

Root-knot nematode (Meloidogyne) Cyst nematode (Heterodera) Root-lesion nematode (Pratylenchus)


Anthracnose (Colletotrichum gloeosporioides) Root rot (Polyporus sulphureus)

African cassava mosaic geminivirus East African cassava mosaic geminivirus Indian cassava mosaic geminivirus

Bacterial blight (Xanthomonas axonopodis pv. manihotis)


Wilt (Fusarium oxysporum f.sp. lentis) Blight (Ascochyta lentis) Rust (Uromyces viciae-fabae) Vascular wilt (Fusarium oxysporum f.sp. lentis) Anthracnose (Colletotrichum truncatum)


Northern corn leaf blight (Helminthosporium turcicum) Downy mildew (Sclerospora and others) Southern corn leaf blight (H. maydis) Rust (Puccinia) Smut (Ustilago zeae) Stalk and ear rots (Gibberella zeae, Diplodia, others)

Chlorotic dwarf machlovirus Streak: geminivirus Yellow dwarf luteovirus

Stewart’s wilt (Erwinia stewartii) Corn stunt disease (Spiroplasma kunkelii)

Common millet

Downy mildew (Sclerospora graminicola)

Finger millet

Blast (Pyricularia setariae) Leaf blight (Cochliobolus nodulosus) (Continued)

Table 5.2 (Continued) Crop





Foxtail millet

Blast (Pyricularia setariae) Rust (Uromyces setariae-italicae) Smut (Ustilago crameri) Downy mildew (Sclerospora graminicola)

Pearl millet

Ergot (Claviceps fusiformis) Downy mildew (Sclerospora graminicola)


Rust (Uromyces eragrostidis) Head smudge (Helminthosporium miyakei)


Crown rust (Puccinia coronata) Stem rust (Puccinia graminis) Powdery mildew (Erysiphe graminis) Smut (Ustilago avenae and U. hordei) Leaf blight (Phaeosphaeria avenaria) Root rot and crown rot (Fusarium) Seedling blight (Glomerella graminicola) Snow mold (Monographella nivalis) Leaf blotch (Pyrenophera avenae) Groat blackening (Alternaria and Cladosporium)

Barley yellow dwarf luteovirus Oat mosaic potyvirus Oat golden stripe furovirus

Halo blight (Pseudomonas syringae pv. coronafaciens)


Early blight (Alternaria solani) Black scurf(Rhizoctonia solani) Late blight (Phytophthora infestans) Pink rot (Phytophthora erythroseptica)

Potato leafroll luteovirus Potato X potexvirus Potato Y potyvirus

Bacterial wilt (Ralstonia solanacearum) Bacterial soft rot (Erwinia carotovora) Common scab (Streptomyces scabies) Bacterial ring rot (Clavibacter michiganensus subsp. sepedonicus)


Blast (Magnaporthe grisea) Brown spot (Cochliobolus miyabeanus) Sheath blight (Rhizoctonia solani)

Rice tungro spherical machlovirus Rice tungro bacilliform badnavirus Barley yellow dwarf luteovirus

Bacterial leaf blight (Xanthomonas oryzae pv. oryzae)


Snow mold (Monographella nivalis) Brown rust (Puccinia recondita) Ergot (Claviceps purpurea) Eyespot (Tapesia yallundae) Sharp eyespot (Rhizoctonia solani) Powdery mildew (Erysiphe graminis) Stem rust (Puccinia graminis) Glume blotch (Phaeosphaeria nodorum)

Barley yellow dwarf luteovirus


Grain molds (Cochliobolus, Fusarium, Mycosphaerella, others) Anthracnose (Glomerella graminicola) Leaf blight (Setosphaeria turcica) Zonate leaf spot (Gloeocercospora sorghi) Tar spot (Phyllachora sorghi) Charcoal rot (Macrophomina phaseolina) Rust (Puccinia purpurea) Ergot (Claviceps sorghi) Downy mildew (Peronosclerospora sorghi)

Maize streak geminivirus


Rust (Phakopsora pachyrhizi) Downy mildew (Peronospora manshurica) Anthracnose (Colletotrichum truncatum and Glomerella glycines) Purple seed stain (Cercospora kikuchii) Pod and stem blight (Diaporthe phaseolorum var. sojae)

Soybean mosaic potyvirus Bean yellow mosaic potyvirus

Sweet Potato

Scab (Sphaceloma batatas) Fusarium wilt (Fusarium oxysporum) Black rot (Ceratocystis fimbriata) Java black rot (Botryodiplodia theobromae) Scurf (Monilochaetes infuscans)

Sweet potato feathery mottle potyvirus

Eelworm (Ditylenchus dipsaci)

Bacterial pustule (Xanthomonas axonopodis pv. phaseoli)

Root-knot nematode (Meloidogyne)

Soil rot (Streptomyces ipomoea) Sweet potato little leaf phytoplasma


Table 5.2 (Continued) Crop




Stem rust (Puccinia graminis f.sp. tritici) Leaf rust (Puccinia recondita f.sp. tritici) Stripe or yellow rust (Puccinia striiformis) Spot blotch (Cochliobolus sativus) Head scab and foot/root rot (Fusarium) Sclerotium foot rot (Corticium rolfsii) Tan spot (Pyrenophora tritici-repentis) Powdery mildew (Erysiphe graminis) Speckled leaf blotch (Mycosphaerella graminicola) Glume blotch (Phaeosphaeria nodorum) Alternaria leaf blight (Alternaria) Loose smut (Ustilago nuda f.sp. tritici) Rhizoctonia root rot (Rhizoctonia)

Barley yellow dwarf luteovirus


Anthracnose (Colletotrichum gloeosporioides) Tuber rots (Fusarium, Penicillium, Rosellinia)

Yam mosaic potyvirus Yam mild mosaic potyvirus


Panama disease (Fusarium oxysporum) Black sigatoka (Mycosphaerella fijiensis)

Banana bunchy top virus (BBTV)

Sources: International Society for Plant Pathology; United Nations Food and Agriculture Organization (FAO).


Bacteria Bacterial leaf streak or black chaff (Xanthomonas translucens pv. undulosa)

Bacterial wilt (Ralstonia solanacearum)

Figure 5.1 Effects of citrus tristeza virus. Source: Photo by S. M. Garnsey. Reproduced with permission from Compendium of Citrus Diseases, 2nd edition, 2000, American Phytopathological Society.



Which Crops Are at Risk? Case Study 5-1: The Secret Life of Aphids The main vector of citrus tristeza is the brown citrus aphid. Unlike most aphids, this species rarely produces a sexual generation. Nearly all brown citrus aphids in North America are females, and they give birth to more females by parthenogenesis (virgin birth). These babies mature in about a week at room temperature and start having more babies. In three weeks, in a world without pesticides or predators, a single aphid could produce at least 4,400 descendants. This lifestyle helps the aphids disperse from one location to another and start new colonies. If the wind blows just one female brown citrus aphid to a new orchard, she can get right down to business without having to look for a mate. And if she happens to be carrying the tristeza virus, so will her thousands of descendants, and they will quickly spread this disease to all the trees where they feed. Even if a farmer manages to kill 90 percent of all aphids in a field, the remaining 10 percent can repopulate the field in a week.

Natural hosts of CTV include orange, mandarin, grapefruit, lemon, and lime trees, plus passionfruit and several less famous tropical fruits (such as Nigerian powder flask, pamburas, and aeglopsis). The most susceptible trees are those grafted on sour orange rootstocks. Other rootstocks, such as Rangpur lime, appear to be resistant. The Numbers

The annual worldwide citrus yield is on the order of 105 million tons, or over 2 billion boxes. In 1981, global losses from CTV alone amounted to 50 million trees. Brazil is the world’s leading producer of citrus crops, with an estimated output of 360 million boxes of fruit in 2007–2008 and about 256 million citrus trees on 2 million acres. The United States is the second largest citrus producer, and Florida produces about 70 percent of the U.S. crop. The Florida citrus harvest varies from year to year, but total production in the 2005–2006 season was about 175 million boxes or 8 million tons, valued at $1.1 billion. Florida has about 621,000 acres planted in citrus. In a normal year, Florida loses about 15 percent of its citrus trees to the citrus tristeza virus. Losses in a major outbreak can exceed 25 percent. History The first citrus trees traveled from Asia to the New World, Europe, and South Africa in the form of seed. Since CTV is not seed-transmitted, the disease did not arrive until later, when growers exported rootstocks in an effort to control other diseases. In the late 1890s, citrus growers in South Africa noticed that trees of sweet orange or mandarin on sour orange rootstock usually died or declined in two or three years. In the 1930s, scientists identified the problem as a viral disease that originated in Japan and followed citrus growers around the world. The new disease reached Brazil in about 1937, and the name tristeza (“sadness”) immediately stuck. By 1950, CTV had destroyed millions of trees in Brazil, Argentina, and southern California. It reached Florida by 1951, where its most efficient vector (the brown citrus aphid) joined it in 1995, thus increasing the potential for damage. As of 2009, farmers in California, Arizona, and Texas anxiously await the arrival of this aphid, which not only transmits CTV but also threatens trees by eating foliage. Prevention and Treatment Once trees are infected, the only known control measure is to destroy the trees. Prevention is complicated, since it requires virus-free budwood and rootstock.



In California, for example, the Citrus Tristeza Virus Interior Quarantine requires any citrus buds, cuttings, or scions to be tested for CTV before a nursery can use them. The California Department of Food and Agriculture (CDFA) maintains an inventory of certified tristeza-free citrus trees, each with a metal tag and identification number. CDFA requires annual tristeza testing; if any registered trees test positive, their registrations are cancelled, but the trees stay in the database. Laws passed in 2008 will further tighten these testing and quarantine requirements by 2010. Popular Culture As oranges gained popularity, scholars of Greek mythology proposed that the life-giving Golden Apples of the Hesperides were really oranges. Thus we have the words hesperidium, meaning any citrus fruit with a thick rind, and hesperidin, a nutrient found in citrus. But the Hesperides were the daughters of Hesperus, the evening star—the planet Venus, seen in the west at sunset—so the fabled orchard should be in the mythic lands beyond the Pillars of Hercules, perhaps in California. In fact, oranges are native to Asia, and Columbus brought them to the New World on his second voyage in 1493. Famous last words are an aspect of popular culture. In 1945, a Texas agronomist wrote: “Standard sour orange has given universally good results as an understock for most varieties of citrus which are produced in this region. There is no reason for suggesting a change at this time, except for the possibility that a destructive disease which destroys trees on sour orange stock may eventually invade this area.”1 The Future There is some evidence that hot weather suppresses the citrus tristeza virus, but it is unlikely that global climate change will help the citrus industry in the long run, because hurricanes and other extreme weather events appear to spread a second disease called citrus canker, discussed later in this chapter.

References and Recommended Reading Bandyopadhyay, R., and P. A. Frederiksen. “Contemporary Global Movement of Emerging Plant Diseases.” Annals of the New York Academy of Sciences, Vol. 894, 1999, pp. 28–36. Bar-Joseph, M., et al. “The Continuous Challenge of Citrus Tristeza Virus Control.” Annual Review of Phytopathology, Vol. 27, 1989, pp. 291–316. Bennett, L. “5,000 Trees Destroyed to Halt Virus.” Los Angeles Times, 26 December 1979. Brlansky, R. H., et al. “Tristeza Quick Decline Epidemic in South Florida.” Proceedings of the Florida State Horticultural Society, Vol. 99, 1986, pp. 66–69. Cambra, M., et al. “Incidence and Epidemiology of Citrus Tristeza Virus in the Valencian Community of Spain.” Virus Research, Vol. 71, 2000, pp. 85–95. Cox, W. “Tristeza Reigns as No. 1 Citrus Foe: Scientists Push Valley Virus Vectors Search.” Fresno Bee, 6 February 1977. Djelouah, K., and A. M. D’Onghia. 2001. “Occurrence and Spread of Citrus Tristeza in the Mediterranean Area.” In Myrta, A., et al. (Eds.), Production and Exchange of Virus-Free Plant Propagating Material in the Mediterranean Region. Bari, Italy: International Center for Advanced Mediterranean Agronomic Studies (CIHEAM). Futch, S. H., and R. H. Brlansky. “Field Diagnosis of Citrus Tristeza Virus.” Gainesville, FL: University of Florida, Institute of Food and Agricultural Sciences, 2005. Kallsen, C. “Controlling the Citrus Tristeza Virus in the San Joaquin Valley of California.” University of California Cooperative Extension, 2 May 2002. 1. Brownsville Herald, 11 November 1945.



Karp, D. “An Orange Whose Season Has Come.” New York Times, 22 January 2003. Marroquin, C., et al. “Estimation of the Number of Aphids Carrying Citrus Tristeza Virus That Visit Adult Citrus Trees.” Virus Research, Vol. 100, 2004, pp. 101–108. Moreno, P., et al. “Citrus Tristeza Virus: A Pathogen That Changed the Course of the Citrus Industry.” Molecular and Plant Pathology, Vol. 9, 2008, pp. 251–268. Nawaz, M. A., et al. “Tristeza Virus: A Threat to Citrus Fruits.” DAWN, 14 July 2008. Reuther, W., et al. (Eds.) 1989. The Citrus Industry. Berkeley: University of California. Rocha-Peña, M. A., et al. “Citrus Tristeza Virus and Its Aphid Vector Toxoptera citricida.” Plant Disease, Vol. 79, 1995, pp. 437–445.

BACTERIAL WILT Summary of Threat Bacterial wilt affects nearly 200 plant species, including potatoes, bananas, tomatoes, peppers, and other important crops. As of 2009, there is no effective treatment other than quarantine and sanitation procedures. The agent (Ralstonia solanacearum) has several strains that affect different plants. One strain (Race 3, Biovar 2) is classified as a biosecurity threat under the Bioterrorism Protection Act of 2002.

Other Names Names include southern bacterial wilt, southern wilt, spur canker, blast, or brown rot (of any affected crop); potato slime disease, jammy eye or sore eye of potato, banana slime disease, banana blood wilt, banana moko disease, tobacco granville wilt, and granville wilt of tobacco. Related bacteria cause Sumatra disease of cloves and bugtok and blood disease in bananas. Bacterial wilt is flétrissement bactérien in French, mörk ringröta in Swedish, and KartoffelSchleimkrankheit in German. Most names in other languages are direct translations, but there are interesting exceptions, such as vaquita de la papa (Spanish, “little cow of the potato”).

Description The agent of this disease is a bacterium (Ralstonia solanacearum) that occurs worldwide and can survive for at least three years in water or soil. It infects over 200 plant species, including staples, cash crops, garden flowers, and wild plants. There are three races with different host ranges: • Race 1 (potato, tomato, pepper, eggplant, legumes, tobacco, other crops) • Race 2 (triploid banana and plantain) • Race 3 (potato, tomato, eggplant, geranium, nettle) Symptoms depend on the host plant and race but usually include discoloration, drooping leaves, and decayed roots, tubers, or fruits (Figure 5.2). Race 1 is endemic in the southeastern United States and many other countries, but it is not considered a quarantine pest. The serious threat is Race 3, biovar 2, which can cause more extensive damage. Besides infecting many different plants, bacterial wilt has several modes of transmission. The agent can enter a plant through the roots or damaged parts, or farm workers can spread it



Figure 5.2 Tobacco plant showing effects of bacterial wilt (Ralstonia solanacearum). Source: Clemson University USDA Cooperative Extension Slide Series, Bugwood.org.

by transporting infected soil on shoes, hands, or tools. The Colorado potato beetle is a mechanical vector for this disease on potatoes. Other insects, birds, and animals that visit host plants may also serve as vectors. Which Crops Are at Risk? Common host plants for bacterial wilt include potato, tomato, banana, plantain, tobacco, red ginger, taro, chili pepper, eggplant, olive, mulberry, peanut, and clove, plus a number of economically important nonfood plants such as castor bean, heliconia, and geranium (Case Study 5-2). Overwatering or heavy rainfall may increase risk. The Numbers Bacterial wilt is one of the world’s most expensive plant diseases. Global losses to the potato industry alone exceed $1 billion per year. In Indonesia, bacterial wilt costs the ginger industry an estimated 75 billion rupiah (U.S. $750,000) per year. This disease is also a major threat to the tomato industry. Worldwide production of tomatoes is about 104 million tons per year, but bacterial wilt can reduce yield by up to 90 percent in India and other endemic areas. History Bacterial wilt disease was first described in 1896 and may be native to the Andean highlands of Peru. Race 3, biovar 2 has not yet become established in the United States or Canada, but it



Case Study 5-2: Geranium Wars In 2003, a greenhouse in Kenya accidentally sent several geranium cuttings infected with Ralstonia solanacearum to a flower producer in California. Later in the year, the same flower producer received a second shipment of infected cuttings, this time from a greenhouse in Guatemala. As a result, more than 900 of the firm’s customers in 47 states received potentially infected plants and were subject to quarantine. The U.S. Department of Agriculture (USDA) requires the destruction of all plants shipped with infected geraniums, so this was an expensive mistake. Worse, since the same disease affects potato, tomato, tobacco, and many other crops, there was a possibility that the bacterium could escape and cost American farmers billions of dollars. About 2 million plants were destroyed, and the eradication was successful. But numerous greenhouses sued the company that made the slip, and the company, in turn, blamed the government for overzealous regulation. This bacterium is on a short list of pathogens that are subject to special reporting requirements under the Bioterrorism Protection Act of 2002, but apparently that fact was unrelated to the USDA’s controversial action, which reflected its mission to block the importation of all plant diseases.

is present in most other potato-growing regions, including Africa, Asia, eastern Australia, Central and South America, and Mexico. It reached western Europe in the 1970s and apparently spread through infected seed potatoes and contaminated irrigation water. This form of bacterial wilt reached the United States in 1999 and 2003 but was successfully eradicated on both occasions.

Prevention and Treatment As of 2009, no known chemical treatment is consistently effective. Some investigators have reported successful control of this disease by inoculating plants with strains of bacteria that inhibit the growth of Ralstonia solancearum. Most control measures focus on the principles of integrated pest management (IPM): Use healthy seed in clean soil, choose disease-resistant or tolerant varieties, graft on resistant rootstocks, and rotate with crops that are not susceptible to bacterial wilt.

Popular Culture

In 2003, the Internet and other media circulated a rumor to the effect that bananas may become extinct within the next ten years because of disease. The source appears to be a controversial report in the journal New Scientist, which focused on two fungal diseases of bananas: black sigatoka and Panama disease. As the rumor grew and improved, moko disease (bacterial wilt) and others were also cited as potential agents of this banana Armageddon. But according to the American Phytopathological Society, the rumor is unfounded. There are many banana strains, and only the Cavendish banana is currently at risk. Also, it would not become extinct, but commercially unviable. (The Cavendish has been America’s favorite banana since the 1960s, when another disease wiped out the much-loved Gros Michel banana. The fact that people were trying to get high by smoking banana peel probably did not help matters either.) Bananas are, however, at greater risk than most fruits, because they produce no seeds and are grown from cuttings. In 2000, an American company claimed that its biopesticide would prevent Ralstonia solanacearum wilt. The product itself was the result of legitimate research at Cornell University, but the aftermath belongs to popular culture. The active ingredient was a bacterial protein that was intended to activate a plant’s immune response. The manufacturer won the EPA’s Green Chemistry Award in 2001—but EPA approval requires only proof that a product is safe, not that it works. When put to the test, the biopesticide was ineffective. The media reported that the



manufacturer sold the technology in 2007, executed a “pump and dump” in 2008, and voted to dissolve. This disappointing outcome should not discourage other companies from trying to develop the effective green technologies that the world so desperately needs.

The Future Bacterial wilt is one of several diseases that may become worse, or more widespread, as a result of global warming (Chapter 6). As a result, the economic impact of bacterial wilt will continue to increase, particularly in those countries least able to afford it. Subsistence farmers have been hit particularly hard in recent years, and better control methods are urgently needed. Since 1992, plant pathologists have organized the International Bacterial Wilt Symposium (IBWS) series to disseminate research findings.

References and Recommended Reading Allen, C., et al. (Eds.) 2005. Bacterial Wilt Disease and the Ralstonia solanacearum Species Complex. St. Paul, MN: APS Press. Aranowski, A. “Plant Pathologists Unpeel Rumors of Banana Extinction.” Press Release, American Phytopathological Society, 14 February 2003. Chalker-Scott, L. “The Myth of the Magic Bullet.” Washington State University, Puyallup Research and Extension Center, April 2005. Daughtry, M. 2003. “Southern Bacterial Wilt, Caused by Ralstonia solanacearum.” Cornell University, Long Island Horticultural Research and Extension Center. Davies, J. C., and B. K. Rubin. “Emerging and Unusual Gram-Negative Infections in Cystic Fibrosis.” Seminars in Respiratory and Critical Care Medicine, Vol. 28, 2007, pp. 312–321. “Detection of Ralstonia solanacearum Race 3 Biovar 2 in New York Greenhouse.” Phytosanitary Alert System, North American Plant Protection Association, 5 January 2004. Eyres, N., and N. Hammond. “Factsheet: Moko Disease Ralstonia solanacearum (Race 2, Biovar 1).” Western Australia Department of Agriculture and Food, 2006. “First Report of Brown Rot on Potato in Ireland.” SeedQuest, 18 October 2007. Floyd, J. 2008. “New Pest Response Guidelines, Ralstonia solanacearum Race 3 Biovar 2.” Riverdale, MD: USDA/APHIS/PPQ. Genin, S., and C. Boucher. “Lessons Learned from the Genome Analysis of Ralstonia solanacearum.” Annual Review of Phytopathology, Vol. 42, 2004, pp. 107–134. Ji, X., et al. “Biological Control Against Bacterial Wilt and Colonization of Mulberry by an Endophytic Bacillus subtilis Strain.” FEMS Microbiology and Ecology, 10 July 2008. Lemay, A., et al. 2003. Pest Data Sheet: “Ralstonia solanacearum Race 3 Biovar 2.” Raleigh, NC: USDA/APHIS/PPQ Center for Plant Health Science and Technology, Plant Epidemiology and Risk Analysis Laboratory. Moorman, G. W. “Bacterial Wilt—Ralstonia solanacearum.” Plant Disease Facts, Pennsylvania State University, Department of Plant Pathology, updated 2008. Prior, P., et al. (Eds.) 1998. Bacterial Wilt Disease: Molecular and Ecological Aspects. New York: Springer. Priou, S., et al. 1999. Integrated Control of Bacterial Wilt of Potato. Geneva: United Nations Food and Agriculture Organization, 16 pp. Smith, E. F. “A Bacterial Disease of Tomato, Pepper, Eggplant and Irish Potato (Bacillus solanacearum nov. sp.).” USDA Division of Vegetable Physiology and Pathology Bulletin, Vol. 12, 1896, pp. 1–28. Stansbury, C., et al. “Bacterial Wilt: Ralstonia solanacearum – Race 3. Exotic threat to Western Australia.” Agriculture Western Australia, Fact Sheet No. 7/2001. “USDA Defends Action.” Gilroy Dispatch, 25 April 2003.



SOUTHERN CORN LEAF BLIGHT Summary of Threat Southern corn leaf blight (SCLB) is a fungal disease that destroyed about 15 percent of the United States maize crop in 1970. Some strains of maize are more susceptible than others, and farmers have largely defeated this disease—for now—by planting resistant strains. The disease has become a favorite of economists and sociologists because of the various principles that its history appears to illustrate. Other Names English names include southern corn leaf blight (SCLB), southern leaf blight of corn, corn leaf blight, southern leaf blight (SLB), southern corn blight, stalk rot, and ear rot. In Spanish, SCLB is la marchitez foliar del maíz del sur or mancha de la hoja del maíz. The French name is helminthosporiose du maïs, and the German equivalent is Blattfleckenkrankheit an Mais. Names for the principal host include Indian corn and maize (Case Study 5-3). Description The infectious agent is a fungus called Cochliobolus heterostrophus (formerly Bipolaris maydis, Helminthosporum maydis, or Drechslera maydis). Its only known hosts are maize or corn (Zea mays) and its relatives teosinte (wild grasses in the genus Zea) and sorghum (Sorghum bicolor and related species). The fungus produces a toxin that prevents the plant from capturing energy from its metabolism, but the virulence of this toxin varies, depending on the race of fungus and the host. The race that caused the 1970 outbreak was called Race T because it produced the T toxin, so named because it attacked specific varieties of hybrid corn with T (Texas) cytoplasm. The predominant strain in the United States now is Race O. Outbreaks have occurred in the Philippines, Asia, Africa, Europe, the United States, and Latin America. Spores disperse by wind or water Case Study 5-3: We Call it Corn droplets and can survive in soil or plant debris In the United States, the word “corn” usuduring the winter. After landing on corn leaves, ally refers to a plant (Zea mays) that the the spores germinate and enter the plant through rest of the world calls maize or Indian corn. stomata. Symptoms include tan lesions on “Corn” is a generic term for the most leaves, sometimes with dark red or purple edges important cereal crop in any region: wheat (Figure 5.3). A black substance may be present in Britain, oats in Scotland, and maize in on the ears, and rot may extend into the interior North America. So whenever this book of the cob. Stalks may also be damaged. refers to corn, it really means maize. Mind you, we aren’t knocking barley, rye, millet, or quadrotriticale. But studies of human hair samples have shown that a startling 70 percent of all the carbon in the body of the average American comes from just one plant: maize. Even people who eat very little “visible” corn absorb a great deal of it in the form of corn syrup and other food and beverage additives.

Which Crops Are at Risk? Only corn with a specific mutation is highly susceptible to southern corn leaf blight. The fungus also attacks other strains of corn, and a few related plants such as teosinte and sorghum, but the effects are less severe. Outbreaks are more likely in hot, wet weather.



Figure 5.3 Cornfield showing effects of southern corn leaf blight. Source: J. K. Pataky, University of Illinois.

The Numbers The southern corn leaf blight outbreak in 1970 destroyed about 15 percent of the U.S. corn crop, causing economic losses estimated at $1 billion or more, depending on the source. At the time, 85 percent of all corn plants in the United States were said to be descendants of one corn plant discovered in Texas in 1944. History Southern corn leaf blight first appeared in the Philippines in about 1962, and its effect on hybrid corn was known by 1969, but it appears that the risk was not taken seriously. After the 1970 disaster, the USDA expected the disease to return in 1971, so they advised farmers to plant more corn than usual to compensate. Some did, others didn’t. Some were unable to get enough resistant seed, so they planted other crops such as milo instead. But the blight caused only minor losses in 1971, and the resulting record corn crop drove down prices. Farmers also wasted money on fungicides. Some analysts later decided that the USDA had acted without sufficient data, but others put a different spin on the same events: In the 1970’s [sic], an unheard-of disease, the southern corn leaf blight, swept through the fields of the Midwest. In a few days, the tall, green, tasseled corn was devastated, as if someone had taken a blowtorch to it. Over that winter, scientists and farmers developed resistant corn varieties in time for the next



spring planting. A national food disaster was stopped dead in its tracks—a triumph of faith, science, and inventiveness.2

The southern corn leaf epidemic of 1970, and the nonepidemic that followed in 1971, are among the few events on record that are regularly cited as both (a) an example of government incompetence and failure, and (b) an example of a magnificent triumph over disease. In 1971, the Associated Press quoted USDA officials to the effect that the corn blight could even dash President Nixon’s hopes for re-election. And in 1972, a number of farmers filed class action suits against major seed companies, alleging that they should have known that T hybrid corn was susceptible to southern corn leaf blight. Apparently, none of these suits ever went to trial. Prevention and Treatment The most effective preventive measure is to plant resistant strains of corn, which are now available worldwide. This strategy has prevented significant outbreaks for many years. Some fungicides are also approved for use, but they are expensive and not always effective, even with repeated applications. Popular Culture In 1970, when southern corn leaf blight wiped out entire cornfields and threatened to devastate the American crop, the message from more than one church pulpit was clear: the blight was yet another tribulation, foretold by the Old Testament story of the seven thin ears blasted by the east wind (Genesis 41). The same vision featured seven lean cows, and some observers noted the spread of the cattle disease rinderpest to the Middle East at about the same time. Other people, however, interpreted the southern corn blight outbreak in less spiritual terms as the result of agroscientists meddling with things best left alone—in this case, the genetic diversity of maize. Yet others found confirmation of their longstanding distrust of the government’s farm policy. And, inevitably, there were those who claimed that Fidel Castro’s legions had sabotaged the U.S. corn crop—just as Castro blamed the United States for outbreaks of dengue fever and Newcastle disease in Cuba during the same era. A natural disaster often serves as a Rorschach test to identify what people are really worried about. The Future This specific disease poses no known risk for the immediate future, but the story of southern corn blight stands as a parable on the dangers inherent in monoculture—in this case, the practice of planting large areas with genetically similar or identical plants that are all vulnerable to the same diseases. This danger is as great today as it was in 1970.

References and Recommended Reading “Corn Blight May Affect Nixon’s Election Hopes for ’72.” Associated Press, 24 January 1971. Gupta, S. “If We Are What We Eat, Americans Are Corn and Soy.” CNN, 22 September 2002.

2. President George (H. W.) Bush, excerpt from remarks to the American Farm Bureau Federation in Orlando, Florida, 8 January 1990.



Hansen, S. F., et al. “Categorizing Mistaken False Positives in Regulation of Human and Environmental Health.” Risk Analysis, Vol. 27, 2007, pp. 255–269. Hooker, A. L. “Studies Related to the Development and Control of the Southern Leaf Blight of Corn Caused by Helminthosporium maydis: Final Report.” Illinois Agricultural Experiment Station, 1976. Kloppenburg, J. R. 2004. First the Seed: The Political Economy of Plant Biotechnology. Madison: University of Wisconsin Press. Levings, C. S. “Thoughts on Cytoplasmic Male Sterility in cms-T Maize.” The Plant Cell, Vol. 5, 1993, pp. 1285–1290. Martinson, C. “Essays on the College of Agriculture’s History: Southern Corn Leaf Blight Epidemic.” Iowa State University, College of Agriculture and Life Sciences, 2007. McGee, D. C. 1988. Maize Diseases: A Reference Source for Seed Technologists. St. Paul, MN: American Phytopathological Society, 150 pp. Miller, R. J., and D. E. Koeppe. “Southern Corn Leaf Blight: Susceptible and Resistant Mitochondria.” Science, Vol. 173, 1971, pp. 67–69. Sindhu, A., et al. 2008. “A Guardian of Grasses: Specific Origin and Conservation of a Unique DiseaseResistance Gene in the Grass Lineage.” Proceedings of the National Academy of Sciences, Vol. 105, 2008, pp. 1762–1767. Smith, N. A. 1972. “Corn Leaf Blights.” Michigan State University, Cooperative Extension Service Bulletin E-832. Tatum, L. A. “The Southern Corn Leaf Blight Epidemic.” Science, Vol. 171, 1971, pp. 1113–1116. Ullstrup, A. J. “The Impacts of the Southern Corn Leaf Blight Epidemics of 1970–1971.” Annual Review of Phytopathology, Vol. 10, 1972, pp. 37–50. Waggoner, P. E. “Epimay: a Simulator of Southern Corn Leaf Blight.” Bulletin, Connecticut Agricultural Experiment Station, 1972, 84 pp. Warren, H. L., et al. “Morphological and Physiological Differences between Bipolaris maydis Races O and T.” Mycologia, Vol. 69, 1977, pp. 773–782.

CITRUS CANKER Summary of Threat Citrus canker may be the world’s most feared disease of citrus crops. The agent is a bacterium that infects citrus trees, discoloring the fruit and making it drop prematurely. It spreads by wind and rain or by contact with infected or contaminated material. Although citrus canker does not usually kill trees outright, it makes the fruit unmarketable and forces removal of infected trees as a control measure. Other Names Citrus canker (CC) is also called citrus bacterial canker (CBC), citrus bacteriosus, or citrus cancrosis. Strains include Asiatic or oriental citrus canker, or cancrosis A; false citrus canker, or cancrosis B; Mexican lime cancrosis, or cancrosis C; citrus bacteriosus, also called Mexican bacteriosus or cancrosis D; and citrus bacterial spot, or cancrosis E. Citrus canker is el chancro de los agrios or úlcera de los cítricos in Spanish, chancre des citrus in French, cancro degli agrumi in Italian, citruskräfta in Swedish, and Zitruskrebs in German. Description The infectious agent is the bacterium Xanthomonas axonopodis (formerly called Xanthomonas campestris, X. citri, Bacillus campestris, Bacterium campestris, Phytomonas campestris, or



Figure 5.4 Grapefruit and leaves showing effects of citrus canker. Source: Timothy Schubert, Florida Department of Agriculture and Consumer Services.

Pseudomonas campestris). It infects most commercially valuable citrus species, and its range is worldwide, although some local areas (such as Queensland, Australia) have eradicated the disease. The agent disperses in water droplets with the help of wind-driven rain. The strains vary by level of virulence and host range. Early symptoms include scablike lesions on fruit (Figure 5.4), often followed by premature fruit drop, loss of leaves, and fatal weakening of the entire tree. Fruit infected with canker is safe to eat but unappetizing in appearance. The worst effects are economic rather than biological. When citrus growers cannot export their fruit because of quarantine restrictions, more fruit ends up in juice, and the price of juice falls. Eventually, citrus canker could force many growers out of business.

Which Crops Are at Risk? Grapefruit, lime, tangerine, orange, lemon, and most other citrus fruits are susceptible to citrus canker. So is the Sichuan pepper tree. Some of the less popular citrus fruits are resistant, such as citron, calamondin, pomelo, and kumquat. An unrelated plant called goatweed, which grows in citrus orchards in India, can serve as a host. Citrus canker causes more damage if an insect called citrus leaf miner (Phyllocnistis citrella) is also present, because its feeding creates breaks in the foliage where bacteria can enter. Other



risk factors include exposure to infected fruit or any contaminated object, such as farm workers’ hands, clothes, tools, or equipment.

The Numbers Between 1984 and 1989, agricultural inspectors in Florida burned an estimated 20 million citrus trees—including many that showed no signs of disease—in an effort to stop a citrus canker outbreak. The cost was about $27 million to the state of Florida and $14 million to the federal government. In 1989, however, officials announced that the disease was not citrus canker after all and budgeted another $20 million to settle lawsuits filed by growers whose stock was destroyed. Interpretations of these events vary. The discovery that citrus canker can spread 580 meters (1,900 feet) during one storm resulted in the “1,900-foot rule,” which required the destruction of all citrus within 1,900 feet of an infected tree. Four hurricanes in 2005 caused $2.2 billion in damage to Florida’s crops and farming infrastructure—including the loss of citrus valued at $180 million—and also spread citrus canker, necessitating the removal of another 10 percent of the state’s citrus groves. By 2005, growers had received an estimated $125 million in compensation. But the biggest number relevant to this discussion is $9 billion, the estimated annual value of Florida’s citrus crop.

History The first reports of citrus canker appeared in Java and India in the mid-nineteenth century. The disease made its debut in Florida in 1911 and spread throughout the Gulf states, but a 20year program eradicated it. The disease turned up again in Florida in the 1980s and was declared eradicated again in 1994. The most recent outbreak, in 1999, set off the most expensive government program ever devoted to a single plant disease (Case Study 5-4). In 2005, following a series of setbacks, the USDA determined that the eradication of citrus canker was essentially impossible, and the effort was formally abandoned in 2006. Management of this disease now focuses on control rather than eradication.

Prevention and Treatment As of 2009, it appears that there is no effective way to treat citrus canker except by removing infected trees. Multiple applications of copper bactericides are sometimes effective, if expensive. The use of windbreaks may also help reduce the dispersal of this disease. Another approach is the use of bacteriophages (viruses that infect bacteria), but the results to date have been disappointing. There are recent reports of improved screening methods that will make it easier to detect bacteria on infected fruit.

Case Study 5-4: Payback Time More than 40,000 residents of Palm Beach County, Florida, reportedly filed a class action suit after state and federal agricultural agencies destroyed their citrus trees in an ultimately futile effort to stop the spread of citrus canker. In 2007 the court awarded them $100 for the first tree lost and $55 for each additional tree. More class action suits were also filed. It is unclear whether this outcome vindicates the people who insisted that the eradication campaign was pointless in the first place.



Popular Culture In 2005, a Florida citrus farmer offered the following prayer during a citrus canker outbreak: “We know that not a sparrow falls to the ground that you don’t know about. We respectfully ask you to take your eyes off the dadburn sparrows and put them on the citrus industry.”3 In 2000, Florida officials agreed to evaluate a product called Celestial Drops or Kabbalah Water as a cure for citrus canker. After six months of testing at taxpayer expense, the product turned out to be plain water, a chemical that Florida already possessed in sufficient quantity. In 2006 and 2008, other entrepreneurs made headlines with similar claims that (as of 2009) have not borne fruit. In the 2005 novel Predator, by Patricia Cornwell, a Florida woman is found murdered after complaining about harassment from a citrus canker inspector. In the words of one reviewer, “You will learn more about citrus canker than you ever wanted to know.” We won’t spoil the ending, but a character named Hog speaks for many Florida residents: “I’ve seen entire orchards burned because of the canker. People’s lives ruined.” In Nancy Cohen’s 2003 novel Highlights to Heaven, some characters discuss issues related to the Florida citrus canker eradication program. Citrus canker is also a theme in Steve Glassman’s 2001 mystery novel The Near Death Experiment, which reportedly is “set against the background of Florida’s orange juice industry.” The Future In the immortal words of Yoda, “Always in motion is the future.” Citrus canker is one of several diseases that are expected to become worse, or more widespread, as a result of global warming (Chapter 6).

References and Recommended Reading Balogh, B., et al. “Control of Citrus Canker and Citrus Bacterial Spot with Bacteriophages.” Plant Disease, Vol. 92, 2008, pp. 2048–2052. Bronson, C. H., and R. Gaskalla. “Comprehensive Report on Citrus Canker in Florida.” Division of Plant Industry, Florida Department of Agriculture and Consumer Services, 15 October 2007. Brown, K. “Florida Fights to Stop Citrus Canker.” Science, Vol. 292, 2001, pp. 2275–2276. “Citrus Canker Outbreak Reported in Australia.” United Press International, 8 July 2004. “Citrus Crop in Danger Due to Disease.” Associated Press, 4 February 2000. “Florida Braces for Small Orange Harvest.” United Press International, 13 July 2006. Golmohammadi, M., et al. “Diagnosis of Xanthomonas axonopodis pv. Citri, Causal Agent of Citrus Canker, in Commercial Fruits by Isolation and PCR-Based Methods.” Journal of Applied Microbiology, Vol. 103, 2007, pp. 2309–2315. Gottwald, T. R. “Citrus Canker: The Pathogen and Its Impact.” Plant Health Progress, August/September 2002. Irey, M., and T. R. Gottwald. “Post-Hurricane Analysis of Citrus Canker Spread and Progress toward the Development of a Predictive Model to Estimate Disease Spread Due to Catastrophic Weather Events.” Plant Health Progress, 22 August 2006. Kennedy, S. “Florida Still Struggles Over the Citrus Canker.” New York Times, 2 July 1989. Layden, L. “Storms Carried Citrus Canker to New Areas Across Florida.” Scripps Howard News Service, 2 March 2005. Li, W., et al. “Genetic Diversity of Citrus Bacterial Canker Pathogens Preserved in Herbarium Specimens.” Proceedings of the National Academy of Sciences USA, Vol. 104, 2007, pp. 18427–18432.

3. Miami Herald, 25 January 2005.



Munson, S. “Loss of Lifestyle after the Hurricane.” Letter to the Editor, Charlotte Sun (Port Charlotte, Florida), 15 January 2009. Salisbury, S. “Citrus Canker Spreads Across State.” Miami Herald, 25 January 2005. Spreen, T. H., and M. L. Zansler. “The Costs and Value Loss Associated with Florida Citrus Groves Exposed to Citrus Canker.” Proceedings of the Florida State Horticultural Society, Vol. 116, 2003, pp. 289–294. Stall, R. E., and E. L. Civerolo. “Research Relating to the Recent Outbreak of Citrus Canker in Florida.” Annual Review of Phytopathology, Vol. 29, 1991, pp. 399–420. Stratton, J. “‘Celestial Drops’ Failed on Canker.” Knight-Ridder/Tribune Business News, 5 July 2005. Sun, M. “The Mystery of Florida’s Citrus Canker.” Science, Vol. 226, 1984, pp. 322–323. Timmer, L. W., et al. (Eds.) 2000. Compendium of Citrus Diseases. 2nd ed. St. Paul, MN: American Phytopathological Society, 92 pp.

LATE BLIGHT OF POTATO Summary of Threat Late blight is a fungus-like organism (an oömycete) that destroys potatoes and related crops. More than one authority has called late blight the worst crop disease in the world. By forcing large-scale use of fungicides, this disease makes potato farming expensive and drives up prices. Late blight caused about 1 million human deaths in Ireland in the 1840s, and now costs the potato industry $3 billion per year. Other Names Names for late blight include potato blight or tomato blight, depending on the crop. In Ireland, late blight was often called mí-adh (pronounced mee-aw, literally “bad luck”). Names that refer specifically to the 1845–1849 late blight epidemic in Ireland include an gorta mór (“the great hunger”) or the potato murrain. It is important not to confuse late blight with early blight, a completely different disease. Description Strictly speaking, the agent of late blight is not a fungus but an oömycete (Phytophthora infestans). Its relatives include the agents of sudden oak death and rhododendron root rot. Until recently, biologists regarded the oömycetes as fungi, members of the same group that includes mushrooms and yeast. Most books still describe late blight as a fungus, and the chemicals used to kill it are usually called fungicides rather than oömyceticides. Late blight is arguably the worst crop disease in the world, infecting potato crops in cool, humid regions of every continent. Although it is now controllable with high levels of fungicide, the cost of treatment has driven up the price of potatoes. If untreated, late blight can still destroy an entire crop in a few weeks. Symptoms include pale green water-soaked lesions that grow into brown or black areas on leaves, stems, and tubers (Figure 5.5). Later, white mold may appear on the underside of leaves, and the potatoes eventually rot. A severely infected field has a distinctive odor. Which Crops Are at Risk? Potatoes are the main crop at risk, although the same disease also affects tomatoes, eggplant, peppers, and a few other crops. The agent will not sporulate (grow spores) if the air is too cold,



Figure 5.5 Potato tuber showing effects of late blight. Source: United Nations Economic Commission for Europe (UNECE).

too hot, or too dry, so farmers use the “temperature-humidity rule” to predict outbreaks. Blight often develops within two or three weeks after a period when the temperature is 50°–80°F (10°–27°C) and humidity is 75 to 80 percent or higher for at least two days. The Numbers Late blight costs the global potato industry an estimated $3 billion per year. In the United States alone, annual losses amount to $200 million to $400 million per year, plus $100 to $200 per acre for fungicides. History The agent apparently originated in the South American Andes and spread from there to Mexico. It reached the northeastern United States by about 1840, and ships transported it to Europe as an accidental passenger. Once established, late blight destroyed potato crops, not only in Ireland but also in Belgium, the Netherlands, France, and England. The late blight pandemic of 1845–1849 (Case Study 5-5) not only caused the deaths of an estimated 1 million Irish people but also forced millions more to emigrate. While many of these refugees tried to distance themselves from anything reminiscent of poverty, others started nationalist movements. Most historians would agree that the Irish Famine changed the world, and some have attributed the European revolutions of 1848 to the failure of the potato and other crops. Ironically, a Belgian scientist named Charles Morren (1807–1858) found an effective control measure in 1845, the first year of the Famine: removing the upper parts of infected potato


plants would save the tubers. But in those preInternet days, most farmers were probably unaware of Dr. Morren’s findings. For the past 150 years, the claim has periodically surfaced that the British government deliberately mismanaged the Famine as part of a campaign of genocide (or Malthusian adjustment) directed at the Irish. We won’t touch this one—but in the words of Irish nationalist John Mitchel, “The Almighty, indeed, sent the potato blight, but the English created the Famine.”4 From Europe the disease spread to Asia and Africa. It continued to be a major problem even after the 1885 invention of the copper fungicide Bordeaux mixture. Some new strains are highly virulent and resistant to fungicides; as a result, late blight is now a re-emerging disease. Major outbreaks occurred in Germany in 1916, in southern Alberta in 1992, and in New Brunswick in 2003.

Prevention and Treatment


Case Study 5-5: Hard Times Imagine that you are a farmer in western Ireland, sitting down to dinner at the end of a hard day in 1845, 6 years after the Night of the Big Wind. Each person at the table receives 14 pounds of potatoes. No, this is not a joke or a typographic error; farming is strenuous, and farm workers eat a lot. Without butter, 14 pounds of cooked potatoes yield about 3,000 calories, not an unreasonable ration for a hardworking adult. But having become dependent on one crop to sustain your family for generations, now imagine the shock of seeing that crop disappear. You still have a few other foods to keep your spouse and nine children alive, such as seaweed, sour milk, salted herring, and congealed cow’s blood mixed with strong butter. Yum! But these foods, once the rural Irish equivalent of antipasto, have never been available in sufficient quantity—except for seaweed, and once the famine starts in earnest, the shore is stripped bare. And so you hit the road in search of food or work, until the famine fever comes.

About 40 years after the Irish Famine, scientists found that a copper sulfate solution called Bordeaux mixture was effective against late blight. Resistant strains later appeared, and scientists countered with multiple applications and new fungicides. As of 2009, these chemicals remain the first line of defense against late blight, but they are expensive. In an effort to reduce cost, scientists are investigating the use of plant essential oils as late blight suppressors. Another, more controversial approach to this problem is the creation of genetically modified potatoes. Popular Culture The nineteenth-century Irish song “The White Potatoes” refers to late blight: It’s a thousand and eight hundred years Forty and six years no lie Since our Savior descended in human form Until the potatoes of the world rotted.5

The germ theory of disease existed in the 1840s, but most people had never heard of it. Thus, when late blight struck Ireland and northern Europe, farmers blamed it on the Evil Eye, the sins of the world, or just mí-adh—bad luck. By Irish tradition, a kettle of boiled potatoes dumped in a neighbor’s field would reduce his crop; in the early days of the potato murrain, 4. John Mitchel, The Last Conquest of Ireland (1861). 5. A. Gribben (Ed.), The Great Famine and the Irish Diaspora in America (University of Massachusetts Press, 1999), pp. 119–120.



many misunderstandings occurred before anyone recognized the extent of the disaster. In Scotland, the potato was already suspect because of its relationship to the toxic nightshades and because the Bible did not mention it. Many celebrated novels refer to the Irish Famine, including Peter Behrens’ The Law of Dreams (2006), Nuala O’Faolain’s My Dream of You (2001), Liam O’Flaherty’s Famine (1937), Anthony Trollope’s Castle Richmond (1860), and William Carleton’s The Black Prophet (1847). Motion pictures about the Famine include The Field (1991) and Untamed (1955).

The Future It is not clear whether global climate change will increase or decrease the range and severity of late blight. In some parts of the world, higher temperatures might reduce opportunities for sporulation; in others, climate change might favor blight by increasing humidity. Public acceptance of genetically modified potatoes and other crops may increase as alternatives fail.

References and Recommended Reading Anderson, P. K., et al. “Emerging Infectious Diseases of Plants: Pathogen Pollution, Climate Change and Agrotechnology Drivers.” Trends in Ecology and Evolution, Vol. 19, 2004, pp. 535–544. Andreu, A. B., et al. “Enhancement of Natural Disease Resistance in Potatoes by Chemicals.” Pest Management Science, Vol. 62, 2006, pp. 162–170. Bandyopadhyay, R., and P. A. Frederiksen. “Contemporary Global Movement of Emerging Plant Diseases.” Annals of the New York Academy of Sciences, Vol. 894, 1999, pp. 28–36. Bhattacharjee, S., et al. “The Malarial Host-Targeting Signal is Conserved in the Irish Potato Famine Pathogen.” PLoS Pathogens, Vol. 2, 2006, p. e50. Cummins, J. “Genes from a Wild Plant Solanum bulbocastanum Used to Resist Potato Blight Fungus.” News Release, GM-Free Ireland, 28 January 2006. Egelko, B., and B. Tansey. “Engineered Alfalfa Ban Upheld on Appeal.” San Francisco Chronicle, 3 September 2008. Froyd, J. D. “Can Synthetic Pesticides be Replaced with Biologically-Based Alternatives? An Industry Perspective.” Journal of Industrial Microbiology and Biotechnology, Vol. 19, 1997, pp. 193–195. Gribben, A. (Ed.) 1999. The Great Famine and the Irish Diaspora in America. Amherst: University of Massachusetts Press. Grunwald, N. J., and W. G. Flier. “The Biology of Phytophthora infestans at Its Center of Origin.” Annual Review of Phytopathology, Vol. 43, 2005, pp. 171–190. Judelson, H. S. “The Genetics and Biology of Phytophthora infestans: Modern Approaches to a Historical Challenge.” Fungal Genetics and Biology, Vol. 22, 1997, pp. 65–76. Kandell, J. “Building a Better Potato.” Los Angeles Times, 11 August 2002. Lee, M. R. “The Solanaceae: Foods and Poisons.” Journal of the Royal College of Physicians, Edinburgh, Vol. 36, 2006, pp. 162–169. O’Callaghan, M. “BASF Admits Defeat of GMO Potato Experiment.” News Release, GM Free Ireland, 24 May 2006. “Potato Blight Threatens New Brunswick Crop.” United Press International, 11 August 2003. Ristaino, J. B. “Tracking Historic Migrations of the Irish Potato Famine Pathogen, Phytophthora infestans.” Microbes and Infection, Vol. 4, 2002, pp. 1369–1377. Ristaino, J. B., et al. “PCR Amplification of the Irish Potato Famine Pathogen from Historic Specimens.” Nature, Vol. 411, 2001, pp. 695–697. Shattock, R. C. “Phytophthora infestans: Populations, Pathogenicity and Phenylamides.” Pest Management Science, Vol. 58, 2002, pp. 944–950. Staples, R. C. “Race Nonspecific Resistance for Potato Late Blight.” Trends in Plant Science, Vol. 9, 2004, pp. 5–6.



Ulman, C., et al. “Zinc-Deficient Sprouting Blight Potatoes and Their Possible Relation with Neural Tube Defects.” Cell Biochemistry and Function, Vol. 23, 2005, pp. 69–72. Varzakas, T. H., et al. “The Politics and Science Behind GMO Acceptance.” Critical Reviews in Food Science and Nutrition, Vol. 47, 2007, pp. 335–361.

SOYBEAN RUST Summary of Threat Soybean rust is a fungal disease that affects soybeans and other legume crops. It can cause defoliation, with losses of 70 to 80 percent. The fungus spreads by windborne spores. As of 2009, there are no resistant soybean strains, and control requires fungicide use. The U.S. government classified soybean rust as a biosecurity threat under the Bioterrorism Protection Act of 2002, but then delisted it again in 2005 to make it easier to study. Other Names English names for this disease include Asian soy or soybean rust (ASR), Australasian soybean rust, Asian rust, and soy rust. Most names in other languages are direct translations: la roya de la soya del Asia or la roya de la habichuela soya in Spanish, la rouille de la soja in French, Asiatischen Sojarosts in German, and Sojabohnenrostes in Swedish. Description “Soybean rust” actually refers to two related diseases. The agent of the more virulent disease is the fungus Phakopsora pachyrhizi, which can cause premature defoliation of soybean plants. Symptoms include small lesions on leaves that turn tan or reddish (Figure 5.6). Older names for this fungus include Phakopsora sojae, P. calothea, Malupa sojae, and Uredo sojae. Another fungus, Phakopsora meibomiae, causes a similar but milder disease. In this book, “soybean rust” means the virulent form unless otherwise specified. Wind, rain, and contaminated objects transmit soybean rust. The disease is most likely to develop in rainy or humid weather, with temperatures between 59°F and 82°F (15°–28°C). The range of soybean rust changes from year to year, but in 2009 it is well established in the United States (16+ states), Mexico, and parts of South America, Asia, Africa, and Australia. Since low winter temperatures and low humidity limit its range, the only part of Europe at risk is the southern Mediterranean region. More than 150 plant species can serve as hosts for soybean rust, including lima beans, blackeyed peas, garden peas, kidney beans, green beans, yam bean, and many common wild plants such as coral bean, clover, locoweed, lupine, and kudzu (Pueraria montana). Kudzu, a huge Asian weed that overruns everything, is resistant to soybean rust and can also survive cold weather. Thus, by infecting kudzu, soybean rust can safely overwinter in the United States. Which Crops Are at Risk? As of 2009, no known soybean strains are resistant to soybean rust. The U.S. crop consists mainly of cultivars that are considered highly susceptible. This plant represents an important part



Figure 5.6 Lesions of soybean rust on underside of leaf. Source: Renato Boff, Universidade Federal do Rio Grande do Sul, Brazil.

of the modern diet; on average, Americans get 10 percent of their daily calories from soybean oil, and the soybean crop is also a major export. Soybean oil turns up in a surprising range of products, such as soaps, paints, insect repellents, herbicides, newspaper ink, and breast implants.

The Numbers In 2005, the United States produced 84 million metric tons of soybeans, of which it exported about 30 percent. The rest of the crop, a mind-numbing 50 million metric tons (over 100 billion pounds), represented domestic consumption. These numbers explain the anxiety that surrounded the 2004 arrival of soybean rust; the United States was the world’s leading producer and consumer of soybeans and in 2005 nearly tied Brazil as the world’s leading exporter. In 2008, the National Agricultural Statistics Service estimated the total U.S soybean crop at 80 million metric tons. Thus far, soybean rust has not had a major impact on production, but the century is young.

History Soybean rust was discovered in Japan in 1902 (Case Study 5-6). It spread to Australia by 1934, India by 1951, Hawaii by 1994, Africa by 1996, and Paraguay by 2001. When it reached Brazil in 2002, scientists realized that its arrival in North America was inevitable. It finally made


its debut in Louisiana and adjacent southeastern states in November 2004, probably with help from Hurricanes Frances and Ivan.

Prevention and Treatment As of 2009, the only preventive measures are chemical control and destruction of weed hosts such as kudzu. Several fungicides are effective, but somewhat expensive. Growers are advised to plant early in the season, with preventive applications of fungicides. Since rust spores adhere to clothing and boots, workers in infected fields should wear disposable spray suits.


Case Study 5-6: The Discovery of Soybean Rust In 1902, Japanese scientist Dr. Torama Yoshinaga (1871–1946) first discovered the soybean rust fungus in a soybean field in Kochi Prefecture on the island of Shikoku. Ironically, soybean rust has never caused serious damage to Japan’s soybean crops, probably because of the country’s cold winters. The soybean plant itself has a long history in Asia. In 2853 B.C., the Chinese emperor Sheng-Nung designated the soybean as one of five sacred plants (the others were rice, wheat, barley, and millet).

Popular Culture According to a peculiar rumor found on the Internet in 2008, the U.S. government imported the South American nutria (a large rodent, plural nutria) to get rid of kudzu—an imported weed that serves as an alternate host for soybean rust. This story makes no sense for three reasons. First, although nutria eat plants, there is no evidence that they prefer kudzu. Second, nutria have a wellauthenticated history: ranchers brought them to the United States (and other countries) from South America in the early 1900s, hoping to create a demand for the fur and meat. When these markets failed to materialize, many captive nutria were liberated and became pests. Third, kudzu was not widespread in the United States until the 1930s, and the U.S. Soil Conservation Service was still advising farmers to plant it for erosion control as recently as the 1950s. Thus, the harmful effects of free-roaming nutria were recognized before the harmful effects of kudzu became apparent. Both species are now the targets of multi-million-dollar eradication programs. The soybean itself is the subject of many popular beliefs. Soy contains chemical compounds similar to the female hormone estrogen, and health-food advocates have claimed both risks and benefits on that basis. Studies have yielded inconsistent results. Some sources insist that soy can cure everything from hot flashes to high blood pressure, whereas others believe that soy depresses the male sex drive and causes breast cancer in women. To the extent that there is any consensus, it appears that soy products are harmless in moderation.

The Future The soybean industry needs cultivars with durable rust resistance—that is, resistance genes that the rust fungus cannot quickly defeat. As of 2009, related studies are in progress in the United States, Brazil, and other countries. The net effect of global climate change on soybean rust is hard to predict, but its range may expand into areas that are presently inhospitable due to cold winters.

References and Recommended Reading “Asian Soybean Rust Identified in Iowa.” Associated Press, 14 March 2007. Bromfield, K. R. “World Soybean Rust Situation.” Pages 481–500 in Hill, L. D. (Ed.). 1976. World Soybean Research. Danville, IL: Interstate Printers and Publishers.



Bromfield, K. R. “Soybean Rust” (monograph). American Phytopathological Society, December 1984, 65 pp. Coblentz, B. “Soybean Rust Battle Takes Look at Kudzu.” Press release, Mississippi State University Office of Agricultural Communications, 1 May 2008. Del Ponte, E. M., et al. “Predicting Severity of Asian Soybean Rust Epidemics with Empirical Rainfall Models.” Phytopathology, Vol. 96, 2006, pp. 797–803. Dorrance, A. E., et al. 2004. Soybean Rust. Ohio State University Extension Fact Sheet. Dorrance, A. E., et al. 2007. Using Foliar Fungicides to Manage Soybean Rust. Columbus: Ohio State University, 112 pp. Feng, P. C., et al. “The Control of Asian Rust by Glyphosate in Glyphosate-Resistant Soybeans.” Pest Management Science, Vol. 64, 2008, pp. 353–359. “Iowa Officials Question Origin of Asian Soybean Rust Sample.” Associated Press, 30 May 2007. Keller, R. “Sentinel Plots Are Key.” AgProfessional, January 2008. Miles, M.R., et al. “Soybean Rust: Is the U.S. Soybean Crop at Risk?” American Phytopathological Society, June 2003. Mueller, D., and D. Engelbrecht. “Soybean Rust Found in an Iowa Field.” Integrated Crop Management, 1 October 2007. Pivonia, S., and X. B. Yang. “Relating Epidemic Progress from a General Disease Model to Seasonal Appearance Time of Rusts in the United States: Implications for Soybean Rust.” Phytopathology, Vol. 96, 2006, pp. 400–407. Ratcliffe, S. T. “Soybean Rust, Phakopsora pachyrhizi and P. meibomiae.” North Central Pest Management Center, 2002. Rytter, J. L. “Additional Alternative Hosts of Phakopsora pachyrhizi, Causal Agent of Soybean Rust.” Plant Disease, Vol. 68, 1984, pp. 818–819. Shaner, G. E., et al. “Preparing for Asian Soybean Rust.” Purdue University Cooperative Extension Service, ID-324, 2005, 16 pp. Skeeles, J. “Soybean Rust Hurting Crops.” Chronicle-Telegram (Elyria, Ohio), 18 January 2005. United States Department of Agriculture. “Feeding America: The Rust Invasion.” Cooperative State Research, Education and Extension Service (CSREES), Partners Video Magazine 17 (on DVD), 2007. Wright, D. “Dispelling Myths about Asian Soybean Rust.” Plant Health Initiative, Summer 2004.

WITCHES’ BROOM DISEASE Summary of Threat Witches’ broom is one of several diseases that attack cacao trees, whose seed pods are the source of cocoa and chocolate. In 1989, this fungus destroyed an estimated 90 percent of Brazil’s cacao crop. It is one of several factors driving the recent increase in chocolate prices. Fungicides are largely ineffective, so farmers must cut off the infected parts of the trees to prevent the release of spores. Other Names The only common English name for this disease and its agent appears to be witches’ broom fungus or witches’ broom disease—“the witch” for short. Brazilian sources call it fungo vassoura-de-bruxa, the Portuguese equivalent. One website calls it “disease of the brush of witch,” probably the result of machine translation. Description The agent is the fungus Crinipellis perniciosa (formerly called Moniliophthora perniciosa or Marasmius perniciosus). Wind, rain, and human activities can disperse the spores; in one reported



case, an outbreak occurred when workers dumped infected plant debris into a river that carried it downstream to other plantations. Related fungi cause other cacao diseases called frosty pod and black pod. Witches’ broom (Figure 5.7) causes an infected tree to send up a spray of random shoots from its flower clusters and branch tips and also infects the pods, making them unusable and reducing bean production. As of 2009, this disease is limited to the New World tropics and has not reached West Africa or Indonesia, the other major cacao-growing areas.

Figure 5.7 Witches’ Broom Fungus (Crinipellis perniciosa), a mushroom that infects cacao trees and reduces yield. Source: Scott Bauer, USDA Agricultural Research Service.



Every time this interesting mushroom rears its head, the press exploits public fears that it will devastate the global chocolate supply. But why is a threat to chocolate somehow more frightening than a threat to soybeans or potatoes? That’s like asking why Ebola attracts so much media attention and pneumonia so little, although Ebola kills few people and pneumonia kills many. Chocolate is news.

Which Crops Are at Risk? Other fungal diseases called “witches’ broom” attack other crops, but the only major crop at risk from Crinipellis perniciosa is the cacao plant. This fungus also infects liana (Arrabidaea verrucosa and others), nightshades (Solanum sp.), and annatto (Bixa orellana). The fungus produces spores at night, in areas with annual rainfall of 60–80 inches (150–200 centimeters), air temperatures in the range 75°F to 80°F (24°–27°C), and relative humidity of 80–90 percent. As of 2009, no genetically resistant cacao strains are known or widely available, and all cacao trees in South America, Central America, and southern Mexico are at risk. In the 1930s, resistant cacao strains were found in Trinidad, but these plants succumbed to more aggressive strains of the fungus in other countries.

The Numbers The total area planted with cacao trees worldwide is about 27,000 square miles (or 70,000 square kilometers). As of 2009, annual retail chocolate sales total about $50 billion. Sales in the United States alone represent more than one-quarter of this total (about $13 billion). Total cacao production in 2003–2004 was about 3.5 million tons, up from 1.5 million tons in 1983–1984. This trend represents an increase in planted areas rather than higher yield. Witches’ broom and other cacao diseases continue to destroy 30–40 percent of the global crop each year, causing annual losses estimated at $2 billion. As a result, chocolate prices increased by nearly 50 percent between 2006 and 2007. About 70 percent of the world’s cacao beans grow in West Africa. The Ivory Coast contributes about 40 percent of the total, mostly from small family farms. By some estimates, if witches’ broom and related fungi ever become established in West Africa, the world will lose at least one-quarter of its chocolate.

History Cacao and its parasites originated in the Amazon basin, where Native Americans cultivated this crop as early as the seventh century A.D. A statement often attributed to the Aztec Emperor Montezuma alleges that a cup of chocolate permits a man to walk for a whole day without food. Christopher Columbus supposedly was the first European to taste chocolate, during his fourth visit to the New World in 1502. Hernán Cortez later introduced chocolate to Europe, where it was an instant success. The use of chocolate spread to the United States in about 1765, and a Dutch inventor introduced the cocoa press in 1828. Witches’ broom disease of cacao was first described in South America in the late 1700s and has been the subject of scientific investigations since the 1890s (Case Study 5-7).



Prevention and Treatment As of 2009, all known fungicides appear to be ineffective against witches’ broom, or else too expensive for large-scale use. Researchers have tried using another fungus as a biocontrol agent to reduce witches’ broom spore production, but results have been inconsistent. Until a better method is found, the most practical way to manage the disease is by removing infected parts of trees. Growers keep the trees short to make pruning easier. Brooms left on the ground can be sprayed with petroleum oil, which makes the surface repellent to rain water and prevents the fungus from producing spores. Popular Culture

Case Study 5-7: Lessons from Chocolate The history of witches’ broom disease contains a bittersweet lesson. In 1930, an early environmentalist named Albert Stoll Jr. wrote, in the context of a brief review of witches’ broom fungus and other major crop diseases, All plant life, so necessary to the welfare of man, appears to go through successive cycles of devastation and immunity from various forms of disease, keeping the scientists continually on the jump to uncover means of combating the menace. No sooner is this accomplished than up bobs an invading army of insects to wreak more vengeance and make the control task the more difficult. Life is a great struggle and the plant world demonstrates this without a doubt.1

As of 2009, chocolate addiction is a moreor-less recognized phenomenon, yet its users can Mr. Stoll was conservation editor of the Detroit News from 1923 to 1950, and his do little to stop the onslaught of witches’ broom efforts were largely responsible for the creand other diseases that imperil the world’s cocoa ation of Isle Royale National Park in Lake supply. One seemingly unavoidable joke is that Superior. the United States government should add chocolate to its growing list of controlled substances, 1 Ironwood Daily Globe, 4 August 1930 so that the trafficking and use of chocolate would become illegal. Its market price would then skyrocket, and with it the incentive and budget for more aggressive disease control measures. (Yes, of course we’re kidding.) Is it true that burning cacao beans or plants can release lethal clouds of hydrogen cyanide? No. Many plants, including cacao, contain cyanide compounds in small quantities and release some cyanide when burned, but at levels far below OSHA permissible exposure limits. The Future One way to solve the problem of witches’ broom fungus would be to reduce global demand for cacao beans, perhaps by improving the quality (and reducing the cost) of chocolate produced in cell culture. Such a breakthrough might impact Third World economies, but that issue has not hindered the development of synthetic vanilla.

References and Recommended Reading Andebrhan, T. “Studies on the Epidemiology and Control of Witches’ Broom Disease of Cacao in the Brazilian Amazon.” Pages 395–402 in Proceedings of the 9th International Cocoa Research Conference, Lome, Togo, 12–18 February 1984. Lagos, Nigeria: Cocoa Producers’ Alliance, 1985. Becker, H. “Fighting a Fungal Siege on Cacao Farms.” Agricultural Research, November 1999. Bowers, J. H., et al. “The Impact of Plant Diseases on World Chocolate Production.” Plant Health Progress, 9 July 2001. Clarence-Smith, W. G. 2000. Cocoa and Chocolate, 1765–1914. New York: Routledge.



Cronshaw, D. K. “Fungicide Application together with Cultural Practices to Control Cocoa Diseases Caused by Crinipellis perniciosa, Monilia roreri, Phytophthora palmivora in Ecuador.” Tropical Agriculture, Vol. 56, 1979, pp. 165–170. Evans, H. C. “Witches’ Broom Disease: A Case Study. Cocoa in South American Countries.” Cocoa Growers Bulletin, Vol. 32, 1981, pp. 5–19. Evans, H. C. “Cacao Diseases—The Trilogy Revisited.” Phytopathology, Vol. 97, 2007, pp. 1640–1643. Evans, H. C., and R. W. Barreto. “Crinipellis perniciosa: A Much Investigated but Little Understood Fungus.” Mycologist, Vol. 10, 1996, pp. 58–61. Fulton, R. H. “The Cacao Disease Trilogy: Black Pod, Monilia Pod Rot, and Witches’-Broom.” Plant Diseases, Vol. 73, 1989, pp. 601–603. Hebbar, P. K. “Cacao Diseases: A Global Perspective from an Industry Point of View.” Phytopathology, Vol. 97, 2007, pp. 1658–1663. “Mars Teams Up with USDA to Improve Cacao Genetics for Pest and Disease Resistance, Better Yields and Climatic Adaptation.” Food Industry News, 18 July 2008. Money, N. P. 2007. The Triumph of the Fungi: A Rotten History. New York: Oxford University Press. Patterson, R. “Recovery from This Addiction was Sweet Indeed.” Canadian Medical Association Journal, Vol. 148, 1993, pp. 1028–1032. Pegler, D. N. “Crinipellis perniciosa (Agaricales).” Kew Bulletin, Vol. 32, 1978, pp. 731–736. Pereira, J. L., et al. “Witches’ Broom Disease of Cocoa in Bahia: Attempts at Eradication and Containment.” Crop Protection, Vol. 15, 1996, pp. 743–752. “Plant Diseases Threaten Chocolate Production Worldwide.” ScienceDaily, 6 June 2006. Ploetz, R. C. “Cacao Diseases: Important Threats to Chocolate Production Worldwide.” Phytopathology, Vol. 97, 2007, pp. 1634–1639. Purdy, L. H., and R. A. Schmidt. “Status of Cacao Witches’ Broom: Biology, Epidemiology, and Management.” Annual Review of Phytopathology, Vol. 34, 1996, pp. 573–594. Samuels, G. J., et al. “Trichoderma stromaticum sp. nov., a Parasite of the Cacao Witches Broom Pathogen.” Mycological Research, Vol. 104, 2000, pp. 760–764. Stoll, A., Jr. “Our Plant Disease Loss.” Daily Globe, 4 August 1930. Tovar Rodriguez, G. “Witches’ Broom in Cacao, Science and Technology.” Agronomia Colombiana, Vol. 3(1/2), 1986, pp. 15–30. van den Doel, K., and G. Junne. “Product Substitution through Biotechnology: Impact on the Third World.” Trends in Biotechnology, Vol. 4, 1986, pp. 88–90. Wheeler, B. E. J., and Mepsted, R. “Pathogenic Variability Amongst Isolates of Crinipellis perniciosa from Cocoa (Theobroma cacao L.).” Plant Pathology, Vol. 37, 1988, pp. 475–488.

PHOMA STEM CANKER Summary of Threat The agents of phoma stem canker are two related fungi that infect cruciferous vegetables (such as broccoli and cauliflower) and canola, which is a major source of vegetable oil and animal feed. These products may not sound as glamorous as chocolate or oranges, but losses from phoma stem canker amount to nearly $1 billion per year and will probably increase as a consequence of global climate change. Other Names Phoma stem canker is also called blackleg of cabbage or crucifers, black stem disease, phoma leaf spot, crucifer canker, or crucifer dry rot. Spanish texts describe it as pie negro (“black foot” or “black stem”), chancro (“canker”), podredumbre seca (“dry rottenness”), or podredum-



bre de raíz, pie y tallo (“rottenness of the root, stem and stalk”). French and German names have similar translations.

Description The agent, a fungus called Leptosphaeria maculans, has an asexual growth form with a different name, Phoma lingam (formerly Sphaeria lingam or Plenodomus lingam). A less aggressive species, Leptosphaeria biglobosa, also causes phoma stem canker. Like most fungal diseases of plants, phoma stem canker spreads by airborne and waterborne spores, as well as by infected seed and debris (Figure 5.8). The spores enter a host plant through wounds or leaf stomata and grow toward the stem, causing damage that reduces market value or kills the plant. Growth is faster at higher temperatures. Phoma stem canker infects cruciferous plants, including canola (oilseed rape), broccoli, turnip, bok choy, rutabaga, cauliflower, Brussels sprouts, cabbage, collards, kale, and others. Some cruciferous weeds, such as mustard, are also susceptible. The world could survive without cruciferous vegetables, but it would be a sadder place. Canola is a major cash crop, the world’s third largest source of vegetable oil (after soy and palm) and one of the few that can grow in colder climates and in winter. Byproducts are also a major source of animal feed.

Figure 5.8 Life cycle of phoma stem canker (blackleg of canola). Source: Canadian Phytopathological Society.



Which Crops Are at Risk? Case Study 5-8: Save the Crucifers Turnips, mustard, and other crucifers were among the first vegetables cultivated by humans. The Chinese have grown these plants for at least 7,000 years. With such a history, it seems likely that the crucifers will survive the onslaught of phoma stem canker, even under conditions of global warming—but they might not survive the double-whammy of phoma stem canker plus the loss of honeybees (Chapter 4). Cruciferous vegetables, unlike many staple crops, depend on honeybees for effective cross-pollination.

Most cruciferous plants are at risk (Case Study 5-8), and outbreaks are most likely in areas with high summer temperatures. Researchers have developed computer models to simulate the interaction of phoma stem canker development with cultural practices (sowing date, crop density, fungicide application, cultivar, nitrogen management) and physical variables such as temperature and rainfall.

The Numbers

In 2006–2007, the world produced about 18 million metric tons of canola oil. Six nations—China, Canada, India, Germany, France, and Britain—have historically accounted for about 80 percent of production. In addition to canola oil, Canada and the United States (mainly North Dakota) are major producers and exporters of canola seed. More than 80 percent of available seed has been genetically modified for increased resistance to herbicides and disease. As of 2008, worldwide annual losses of canola from phoma stem canker total about $900 million. History The official discoverer of phoma stem canker was German botanist H. J. Tode (1733–1797), who found it on dead cabbage stems and published a description in 1791. The recent history of this disease is mainly about the relative distribution of the two pathogens Leptosphaeria maculans (LM) and L. biglobosa (LB). As of 2005, LM was the predominant species in western Europe and was also present in the United States, Canada, Australia, and parts of Africa. LM appeared to be spreading eastward in 2005 and was present in most eastern European countries, but was absent from Russia. LB was present in North America, Europe, Australia, and part of China. Prevention and Treatment Until recently, the main prevention strategy was to use resistant cultivars. Unfortunately, the fungus has evolved, too, causing major epidemics in Australia and Europe. While studies of genetic resistance continue, fungicides are the main defense, combined with integrated pest management practices such as four-year crop rotation and the avoidance of infected sites. Early detection and treatment are essential, because once the fungus reaches the plant stem, fungicides are no longer effective. Popular Culture We did not expect to find any novels about cruciferous vegetables, but we were wrong. In Don Lee’s acclaimed 2008 novel Wrack and Ruin, the main character is a northern California organic Brussels sprout farmer who must deal with the numerous diseases that afflict his crop.



According to a particularly silly urban legend, turnips and other cruciferous vegetables are never canned because they are treated with chlorine to kill fungus—possibly including Leptosphaeria—and the chlorine would interact with the lining of the can to release deadly chlorine gas. This is false. Many vegetables are washed in a chlorine solution, but it’s rinsed off again before packaging. Gas bubbles sometimes form inside cans of food due to spoilage, but these gases are harmless, and the solution is to throw the cans away or take them back to the store. Turnips, cauliflower, and related vegetables are rarely canned because of their somewhat mushy texture, but we have talked to people who have seen and even eaten canned turnips.

The Future Just when it seemed that global warming was responsible for everything, the press added one more negative consequence to the list. A 2007 study showed that a warmer (and possibly wetter) climate will probably increase the range and severity of phoma stem canker, thus reducing the world’s supply of canola oil, and raising its price at the very time when renewable biodiesel fuels are likely to be in greater demand. The distribution of this disease will move northward into regions that are presently too cold, thus posing a serious risk to subsistence farmers in some parts of China and India.

References and Recommended Reading Aubertot, J.-N., et al. “SimCanker: A Simulation Model for Containing Phoma Stem Canker of Oilseed Rape through Cultural Practices.” Proceedings of the Fourth International Crop Science Congress, Brisbane, Australia, 2004. Delaplane, K. S., and D. F. Mayer. 2000. Crop Pollination by Bees. New York: CABI Publishing. Egan, J., et al. “Burning Canola Stubble May Not Control Blackleg.” Oilseed Outcomes, Oilseed Industry and Agronomic Research Updates, July 2006, No. 1. Evans, N., et al. “Range and Severity of a Plant Disease Increased by Global Warming.” Journal of the Royal Society Interface, Vol. 5, 2008, pp. 525–531. Fitt, B. D. L., et al. “World-Wide Importance of Phoma Stem Canker (Leptosphaeria maculans and L. biglobosa) on Oilseed Rape (Brassica napus). European Journal of Plant Pathology, Vol. 114, 2006, pp. 3–15. Henderson, M. P. “The Black-Leg Disease of Cabbage Caused by Phoma lingam (Tode) Desmaz.” Phytopathology, Vol. 8, 1918, pp. 379–431. Howlett, B. J., et al. “Leptosphaeria maculans, the Causal Agent of Blackleg Disease of Brassicas.” Fungal Genetics and Biology, Vol. 33, 2001, pp. 1–14. Keri, M., et al. “Inheritance of Resistance to Leptosphaeria maculans in Brassica juncea.” Phytopathology, Vol. 87, 1997, pp. 594–598. Marcroft, S. “Australian Blackleg Management Guide.” Canola Association of Australia, January 2005, 4 pp. Markell, S., et al. “Blackleg of Canola.” Fargo: North Dakota State University Extension Service, June 2008, 4 pp. Moreno-Rico, O., et al. “Characterization and Pathogenicity of Isolates of Leptosphaeria maculans from Aguascalientes and Zacatecas, Mexico.” Canadian Journal of Plant Pathology, Vol. 23, 2001, pp. 270–278. Murdock, L., et al. 1991. “Canola Production and Management.” University of Kentucky, College of Agriculture.



Pedras, M. S. C., and Y. Yu. “Stress-Driven Discovery of Metabolites from the Phytopathogenic Fungus Leptosphaeria maculans: Structure and Activity of Leptomaculins A-E.” Bioorganic & Medicinal Chemistry, Vol. 16, 2008, pp. 8063–8071. Rimmer, S. R., et al. (Eds.). Compendium of Brassica Diseases. St. Paul, MN: American Phytopathological Society Press. Sosnowski, M., et al. 2001. “Symptoms of Blackleg (Leptosphaeria maculans) on the Roots of Canola in Australia.” New Disease Reports, Volume 3, July 2001. Sprague, S. J., et al. “Pathways of Infection of Brassica napus Roots by Leptosphaeria maculans. New Phytologist, Vol. 176, 2007, pp. 211–222. Taylor, J. L. “A Simple, Sensitive, and Rapid Method for Detecting Seed Contaminated with Highly Virulent Leptosphaeria maculans.” Applied Environmental Microbiology, Vol. 59, 1993, pp. 3681–3685. West, J. S., et al. “Epidemiology and Management of Leptosphaeria maculans (Phoma Cell Canker) on Oilseed Rape in Australia, Canada and Europe.” Plant Pathology, Vol. 50, 2001, pp. 10–27.

ASIAN SOYBEAN APHID Summary of Threat Asian soybean aphids (Aphis glycines) destroy plants by reproducing in large numbers and eating leaves. They also spread several viral plant diseases. Hosts for this aphid include soybean plants and other legumes, such as snap beans. Recent economic losses in the United States alone have approached $1 billion per year due to crop losses and the cost of pesticides.

Other Names Common English names include exotic soybean aphid, soya bean aphid, SBA, or soy aphid. In other languages, this insect is áfido de la soya (Spanish), puceron du soja (French), Sojabohnenblattlaus (German, “soybean leaf louse”), soijakirva (Finnish), and daizu-aburamusa (Japanese).

Description The soybean aphid (Aphis glycines) is an agricultural pest that has spread from Asia to all major soybean-producing regions of the world. It can reduce soybean yields by up to 50 percent by destroying plants directly, and it also spreads viral diseases such as soybean mosaic virus (SMV), soybean dwarf virus, cucumber mosaic virus, bean yellow mosaic virus, clover yellow vein virus, peanut mottle virus, and potato virus Y. Soybean aphids are tiny greenish-yellow insects with reddish-brown eyes (Figure 5.9). They look similar to two other aphid species that live on the same host plants (Aphis gossypii and A. nasturtii), but the soybean aphid is the only one that forms large colonies. When conditions become crowded, soybean aphids produce a generation of winged adults that can fly to new fields. Wind and rain may also disperse these insects. In North America, winter hosts include a woody shrub called common buckthorn (Rhamnus cathartica) and the Asian weed kudzu (Pueraria montana).



Figure 5.9 Asian soybean aphid. Source: Purdue University.

Unlike the brown citrus aphid (Case Study 5-1), the Asian soybean aphid has a sex life during part of the year. In summer, the entire population is female. In fall, both males and females are born, some of them with wings. The aphids migrate from soybeans to buckthorn shrubs, where they mate and lay their winter eggs. The eggs hatch in spring, and two or three generations of aphids live on buckthorn before returning to the soybean plants.

Which Crops Are at Risk? Soybeans are the main crop at risk, but Asian soybean aphids can also infest snap beans and possibly alfalfa. In soybeans, yield loss depends partly on the stage of growth when the aphid infestation occurs. If aphid density is high when the soybean plants begin to flower, the damage is greatest, because the aphids interfere with pod development. Damage is also greater if plants are unhealthy due to dry soil or other unfavorable conditions. Aphids reproduce most rapidly at air temperatures of 75°–80°F (24°–27°C), and tend to stop reproducing when the mercury hits 90°F (32°C). Predators, parasites, some fungi, and thunderstorms can reduce aphid populations. The Numbers Between 2001 and 2004, the soybean aphid cost the U.S. economy an estimated $2.2 billion in crop losses, pesticides, and biological control programs. Each female soybean aphid has about



45 offspring, called nymphs, over a period of 15 days in summer. These nymphs become adults in about 5 or 6 days. The number of soybean aphids per plant required to cause economic damage may range from 2,500 to 4,000, depending on weather and other conditions. One Asian ladybird beetle can eat 160 aphids per day. History The Asian soybean aphid is native to eastern Asia. It arrived in the United States sometime before 2000, probably on airline passengers or horticultural cargo from Japan or China. The species was first identified in Wisconsin in the summer of 2000, and by 2003 it had spread to at least 20 states by active and wind-aided flight, and possibly also by clinging to vehicles. The reported distribution varies from year to year, but the species has occupied most soybeangrowing areas. Prevention and Treatment Case Study 5-9: Alien Versus Predators When the Asian soybean aphid arrived in the United States in 2000, it became food for many predators, including the multicolored Asian lady beetle, which the USDA had already imported in the hope of controlling other aphids. By 2004, at least 22 predator species (native and nonnative) were eating Asian soybean aphids, yet outbreaks continued, often reducing soybean yield by as much as 40 percent. Scientists are now studying an Asian parasitic wasp called Binodoxys communis to see if it might serve as a form of biological control. It can kill Asian soybean aphids, but the problem is that it might compete with Asian lady beetles and other predators, instead of augmenting their efforts.

Insecticides are the main control method, but these chemicals also kill beneficial insects and increase production costs. Studies of biological control methods have yielded some promising results (Case Study 5-9). For example, certain plants used as living mulches can increase populations of predators that eat aphids. Other control strategies include the use of resistant varieties, reflective mulches (because ultraviolet light deters winged aphids), trap cropping, weed control, rouging, and mineral oil sprays. Since soybean aphids spend the winter on buckthorn shrubs, one obvious approach is to remove buckthorn near soybean fields. This is not as easy as it might sound, because buckthorn quickly regrows from a cut stump. Popular Culture

Aphid folklore is surprisingly rich, perhaps because of the long association between aphids and farmers. In the Hebrides Islands of Scotland in the nineteenth century, children learned to extract honeydew by placing aphids on the backs of their hands and reciting a Gaelic poem, rendered in English as follows: Carlin of the whey, Whey-pail, whey-pail, Give me of your whey Or I will take head and feet off you.6 6. A. Goodrich-Freer, “More Folklore from the Hebrides” (Folk-Lore, Vol. 13, 1902, pp. 29–62).



In response to this ritual, the aphid would deposit a drop of sweet liquid on the child’s hand. (This actually works.) According to a legend of uncertain provenance, medieval European farmers once prayed to the Virgin Mary to rescue their crops from aphids. Swarms of small red beetles soon appeared and ate the aphids, thus saving the crops and preventing a famine. From that day forward, these insects were known as the beetles of Our Lady, Our Lady’s bird, lady beetles, ladybirds, or ladybugs. Each lady beetle had seven black spots, representing the seven sorrows of the Blessed Virgin. In real life, the number of spots on a lady beetle may range from 0 to 24; a common European species has seven spots. But part of this story predates the Christian era, for the lady beetle was also associated with Freyja, the Norse mother goddess. The ladybug has inspired other legends, judging by its many unusual English names: fly-golding, goldie-bird, Bishop Barnaby, or God’s almighty cow. Its Italian name means “the devil’s chicken,” whereas a more practical German name translates as “little hemispherical beetle.”

The Future Soybean aphid outbreaks are rare in the species’ native China, thanks to the presence of parasitic wasps and other natural enemies, but it is impossible to recreate an entire foreign ecosystem piece by piece. Although further study may yield more effective biological controls, pesticides and the associated costs are likely to be necessary for the foreseeable future.

References and Recommended Reading Aponte, W., and D. Calvin. “Fact Sheet: Soybean Aphid (Aphis glycines).” Penn State Entomology Department, July 2004. “Bacteria Protect Soybeans from Aphids.” United Press International, 14 April 2009. Blackman, R. L, and V. F. Eastop. 1984. Aphids on the World’s Crops: An Identification and Information Guide. New York: John Wiley. Diaz-Montano, J., et al. “Chlorophyll Loss Caused by Soybean Aphid (Hemiptera: Aphididae) Feeding on Soybean.” Journal of Economic Entomology, Vol. 100, 2007, pp. 1657–1662. Griffiths, P. D. “Evaluation and Enhancement of Virus-Resistant Snap Beans.” Final Project Report, NYS IPM Program, 2006. Heimpel, G. E. “Soybean Aphid as Part of a Potential Four-Species Invasional Meltdown: Evaluation and Implications for Management.” Abstract of paper presented at Ecological Society of America Annual Meeting, 16–19 November 2008. Hill, C. B., et al. “Resistance of Glycine Species and Various Cultivated Legumes to the Soybean Aphid (Homoptera: Aphididae). Journal of Economic Entomology, Vol. 97, Vol. 2004, pp. 1071–1077. Landis, D. A., et al. “Impact of Multicolored Asian Lady Beetle as a Biological Control Agent.” American Entomologist, Vol. 50, 2004, pp. 153–154. McCormack, B. P., et al. “Demography of Soybean Aphid (Homoptera: Aphididae) at Summer Temperatures.” Journal of Economic Entomology, Vol. 97, 2004, pp. 854–861. McGraw, L. “New Aphid Threatens U.S. Soybeans—Aphis glycines.” Agricultural Research, May 2002. Miao, J., et al. “Population Dynamics of Aphis glycines (Homoptera: Aphididae) and Impact of Natural Enemies in Northern China.” Environmental Entomology, Vol. 36, 2007, pp. 840–848. Myers, S. W., et al. “Effect of Soil Potassium Availability on Soybean Aphid (Hemiptera: Aphididae) Population Dynamics and Soybean Yield.” Journal of Economic Entomology, Vol. 98, 2005, pp. 113–120. Nault, B. A. “Aphid Ecology and Epidemiology of Cucumber Mosaic Virus in Snap Bean Fields: Implications for Management.” Cornell University, March 2007.



O’Neil, R. “Biological Control of the Soybean Aphid.” SABC Annual Report to North Central Soybean Research Program, April 2007. “Reuniting Old Enemies: Releasing Aphid Enemies from Asia into Midwest Soybean Fields.” Urbandale: Iowa Soybean Association, 2007. Schmidt, N. P., et al. “Alfalfa Living Mulch Advances Biological Control of Soybean Aphid.” Environmental Entomology, Vol. 36, 2007, pp. 416–424. Shah, D. A., et al. “Incidence, Spatial Patterns, and Associations among Viruses in Snap Bean and Alfalfa in New York.” Plant Disease, Vol. 90, 2006, pp. 203–210. Sloderbeck, P. E., et al. “The Soybean Aphid.” Kansas State University Agricultural Experiment Station and Cooperative Extension Service MF-2582, June 2003. Takahashi, S., et al. “Life Cycle of the Soyabean Aphid Aphis glycines Matsumura, in Japan.” Japanese Journal of Applied Entomology and Zoology, Vol. 37, 1993, pp. 207–212. Wang, X. B., et al. “A Study on the Damage and Economic Threshold of the Soyabean Aphid at the Seedling Stage.” Plant Protection, Vol. 20, 1994, pp. 12–13. Wyckhuys, K. A. G., et al. “Parasitism of the Soybean Aphid Aphis glycines by Binodoxys communis: the Role of Aphid Defensive Behavior and Parasitoid Reproductive Performance.” Bulletin of Entomological Research, Vol. 98, 2008, pp. 361–370.

LOCUSTS Summary of Threat Locusts are grasshoppers that migrate in huge swarms, destroying crops in their path. A single swarm may be several miles long and may devastate a field in minutes. Natural predators and parasites help reduce locust numbers. Other control measures include insecticide spraying from vehicles and plowing the soil to destroy locust eggs. Better methods are needed, particularly in Africa and the Middle East. Other Names English nicknames and euphemisms for locusts include “the countless,” “darkener of the sun,” “shrimp of the desert,” “flying shrimp,” or “hopper.” In other languages, locusts are anbeta (Ethiopian), saltamontes (Spanish), sauterelle (French), cavalletta (Italian), gafanhoto (Portuguese), si-khónyane (Swazi), adede (Luo), luzige (Egyptian), sprinkaan (Afrikaans), Woestijnsprinkhaan (Dutch), or Heuschrecke (German). Description Locusts are grasshoppers that sometimes come together in huge migratory swarms. In some species, this swarming follows a physical transformation that results from crowding. Of about 8,000 grasshopper species, only 10 or 12 are known to have a locust phase. The most famous is the desert locust (Schistocerca gregaria), shown in Figure 5.10. This insect occurs throughout Africa, the Middle East, and western Asia—about 20 percent of the land surface of the Earth. China, South America, Australia, and other major agricultural areas have their own locust species. Some closely related grasshoppers occur in the United States, but they do not swarm, although they can cause severe crop damage.



Figure 5.10 Desert locust (Schistocerca gregaria). Source: Spencer Behmer, Texas A&M University.

Which Crops Are at Risk? All plants (and wooden objects and laundry) in the path of a migratory locust swarm are at risk. In some parts of the world, locust swarming is associated with high seasonal rainfall. The effects of temperature are less clear; warmer winters may enable locusts to survive, but hotter summers may be less favorable.

The Numbers A single desert locust swarm can contain as many as 80 million locusts per square kilometer, or 31 million per square mile. The swarm may contain billions of locusts, and it can travel more than 81 miles (130 kilometers) per day, destroying more than 100 tons of vegetation every day. One reported locust swarm in Africa was about 1 mile (1.6 km) wide at the front and 100 feet (about 30 meters) high, and took more than nine hours to pass overheard. But according to an 1880 report, a swarm of Rocky Mountain locusts in 1875 was much larger—an astonishing 110 miles (176 km) wide and 1,800 miles (2,880 km) long. When China had a locust outbreak in 2008, a few weeks before the Olympic Games, the government sent 33,000 professional exterminators to contain the problem. But large-scale pesticide spraying causes other problems. By one estimate, there are over 25 million cases of work-related pesticide poisoning in developing countries every year.



History The phenomenon of locust swarming is older than agriculture, but we will fast-forward for the sake of brevity. Examples of major outbreaks occurred in the United States in 1875; in Palestine in 1915; in South America in 48 of the 58 years between 1897 and 1954, but apparently none since; in Africa in 1986–1989 and 2004; in Australia in 2004; and in China in 2008. Only once in the history of agriculture has mankind succeeded in driving a pest to extinction, and even that victory resulted from an accident. Rocky Mountain locusts (Melanoplus spretus) in the Great Plains aggregated in some of the largest swarms ever described, but by the early twentieth century they were extinct. Studies of frozen locusts in glaciers revealed the probable sequence of events: Although the invasion area of this locust was over 2 million square miles (5.5 million square kilometers), the areas where it laid its eggs were quite small, and were limited to river valleys where settlers grazed their cattle and plowed the soil. In so doing, they inadvertently wiped out the locust’s underground nursery. Prevention and Treatment For more than a thousand years, the Chinese have kept records of locust activity and weather conditions in an effort to predict swarming. Other countries later adopted a similar approach using GIS technology and satellite imagery, but the result is the same. Tracking the movement of locust swarms and preparing for their arrival is an important component of prevention. Farmers in Africa use vehicle-mounted and aerial insecticide sprayers to protect crops from locusts, which acquire the chemicals when they land on the plants and start eating them. Biopesticides—bacteria, fungi, pheromones, and plant extracts such as neem—work more slowly than chemical pesticides, but cause less harm to people and the environment. Natural enemies of locusts include birds, reptiles, and certain parasitic or predatory wasps, flies, and beetle larvae. Digging up locust eggs might work in theory, but in most regions this approach is impracticable because of the size of the area affected. Popular Culture The 1957 motion picture Beginning of the End is about giant man-eating grasshoppers, created by accident when ordinary grasshoppers get into a silo full of radioactive wheat at an experimental farm in Illinois. The scientists, who have tampered with forces best left alone, wring their hands until the Army comes to the rescue. Our favorite line, spoken by the General: Dr. Wainwright, you’re a scientist, you know what grasshoppers can do. I’m a soldier, I know what guns can do.

In the 1950s, journalists speculated about the possibility of using radiation to create better crops and livestock, and this prospect inspired the same fears that resulted from genetic engineering experiments a generation later. But there is nothing unbelievable about grasshoppers suddenly becoming huge (at least collectively) and causing widespread destruction. Locusts do it all the time. In the 2004 motion picture Hidalgo, desert locusts serve as food for the hero and his horse (see also Case Study 5-10, page 189). In many places where locusts occur, they are not the worst natural phenomena that farmers must deal with. An Ethiopian proverb holds that “It is better to have locusts than rain in November.”7 (Rain promotes mold, which can destroy grain stored after the fall harvest.)


In her 1937 memoir On the Banks of Plum Creek, Laura Ingalls Wilder (famous for Little House on the Prairie) vividly described a swarm of Rocky Mountain locusts attacking a wheat field. This species now appears to be extinct.

The Future In 2009, researchers reported that a chemical called serotonin causes grasshoppers to transform into locusts. Someday it might be possible to develop chemical weapons that specifically block this transformation by inhibiting serotonin production in grasshoppers. But since serotonin is also a neurotransmitter in the brains of many other animal species—including humans— extensive testing will be required to ensure safety. Otherwise, the potential for urban legends, science-fiction novels, and real-life tragedy is immense.

References and Recommended Reading


Case Study 5-10: Deep-Fried Locust In the fifth century B.C., the historian Herodotus wrote that people in the region we now call Libya ate powdered locusts mixed with milk. More recently, John the Baptist and the prophet Muhammad ate locusts. Dried locusts contain up to 75 percent protein and are rich in B vitamins. Here is a modern recipe, courtesy of the Peace Corps. Ingredients: Vegetable oil, locusts, salt, and chili powder. Go out at night in locust season, wearing a headlamp, and grab handfuls of locusts that are attracted to the light. Put them in a bag and take them back to the kitchen. Pull off the wings, wash the locusts, and pat dry. Then fry the locusts for about two minutes in hot vegetable oil, and put them on a plate with a paper towel to absorb excess oil. Sprinkle with chili powder and salt. (The Peace Corps also recommends putting the plate out in the sun to make the locusts crunchy, presumably with a cover to keep flies from landing on it.) In the United States, lubber grasshoppers are reportedly good to eat, although harvesting them is more labor-intensive because they do not swarm. Also, it is important to avoid eating grasshoppers that have been sprayed with pesticides. Other traditional locust or grasshopper recipes include boiling, roasting, stewing in butter, or mixing ground-up locusts with flour and water and baking them into cakes.

Bhattacharya, S. “Plague of Locusts Causes Mass Allergy Attack.” Sudan Tribune, 12 December 2008. Buhl, J., et al. “From Disorder to Order in Marching Locusts.” Science, Vol. 312, 2006, pp. 1402–1406. Bukkens, S. G. F. “The Nutritional Value of Edible Insects.” Ecology of Food and Nutrition, Vol. 36, 1997, pp. 287–319. Ceccato, P., et al. “The Desert Locust Upsurge in West Africa (2003–2005): Information on the Desert Locust Early Warning System and the Prospects for Seasonal Climate Forecasting.” International Journal of Pest Management, Vol. 53, 2007, pp. 7–13. Enserink, M. “Can the War on Locusts Be Won?” Science, Vol. 306, 2004, pp. 1880–1882. Harmon, K. “When Grasshoppers Go Biblical: Serotonin Causes Locusts to Swarm.” Scientific American, 30 January 2009. Levy, S. “Last Days of the Locust.” New Scientist, 21 February 2004. Lockwood, J. 2004. Locust: The Devastating Rise and Mysterious Disappearance of the Insect That Shaped the American Frontier. New York: Basic Books, 304 pp. “Locust Army Gathers in Africa.” New Scientist, 11 September 2004. “Locust Plague Sweeps South, Swarming Desert Capital.” Associated Press, 6 August 2004. Lomer, C. J., et al. “Biological Control of Locusts and Grasshoppers.” Annual Review of Entomology, Vol. 46, 2001, pp. 667–702. Lovejoy, N. R., et al. “Ancient Trans-Atlantic Flight Explains Locust Biogeography: Molecular Phylogenetics of Schistocerca.” Proceedings Biological Sciences, Vol. 273, 2006, pp. 767–774. 7. J. McCann, People of the Plow (Univ. of Wisconsin Press, 1995).



Magnier, M. “Add Locusts to China’s List of Calamities.” Los Angeles Times, 3 July 2008. “Mali Calls for Help to Fight Locust Swarms.” Reuters, 25 July 2004. Miller, G. A., et al. “Swarm Formation in the Desert Locust Schistocerca gregaria: Isolation and NMR Analysis of the Primary Gregarizing Agent.” Journal of Experimental Biology, Vol. 211, 2008, pp. 370–376. “North Africa Wars on Locusts.” Associated Press, 22 April 1988. Peatling, S. “Australia Braces for Locust Plague.” National Geographic News, 30 November 2004. Prior, C. “Locust and Grasshopper Biocontrol with Fungi.” Mycological Research, Vol. 108, 2004, p. 724. Ullman, M. “African Desert Locusts in Morocco in November 2004.” British Birds, Vol. 99, 2006, pp. 489–491. Whiting, J. D. “Jerusalem’s Locust Plague.” National Geographic, December 1915.

CONCLUSION: ONE TO GROW ON There are hundreds of known plant diseases and pests, and nobody knows which ones will next emerge in a new and threatening form. Perhaps the most dreaded new candidate is a highly virulent, fungicide-resistant strain of a disease called black stem rust of wheat (Figure 5.11). This

Figure 5.11 Ug99 strain of wheat rust on wheat in Njoro, Kenya. Source: Yue Jin, USDA Agricultural Research Service.



disease caused huge losses and famines in the first half of the twentieth century, but resistant wheat strains kept it under control. Now, it appears to be back. The new strain is called Ug99 because it was discovered in Uganda in 1999. Reports indicate that Ug99, if not contained, is capable of destroying 10 percent of the world’s wheat production. It spread to Kenya by 2002 and to Ethiopia by 2003. As predicted, it reached Sudan and Yemen in 2006, and Iran by 2007. Inevitably, it will spread to the rest of Asia and the Americas. Remedial action is in progress; a Global Rust Initiative has been established in Nairobi to monitor the progress of the disease and to develop resistant wheat.

References and Recommended Reading “Bayer CropScience Fungicides Have Proven Control of Ug99 in Wheat Trials.” Press release, Bayer CropScience, 19 June 2008. Borlaug, N. E. “Stem Rust Never Sleeps.” New York Times, 26 April 2008. “Fungus Puts World Wheat Crop at Risk.” United Press International, 27 March 2008. Lacey, M. “New Strain of Wheat Rust Appears in Africa.” New York Times, 9 September 2005. Mackenzie, D. 2007. “Billions at Risk from Wheat Super-Blight.” New Scientist Environmental, 3 April 2007. “Scientists Fight Stem Rust UG99 before It Becomes a Threat.” PhysOrg.com, 18 November 2008. “Ug99 Now in Iran.” Geneva: United Nations Food and Agriculture Organization, News Release, 5 March 2008.

This page intentionally left blank


Making Things Worse

We have met the enemy and he is us. —Walt Kelly, 1970 Pogo cartoon

Biological threats do not exist in a vacuum. The topics in this chapter include physical, chemical, and sociological factors that increase the level of risk associated with some of the diseases discussed in Chapters 2 through 5. These accessory threats are often controversial, and most have no easy solutions.

TOO MANY BABIES: OVERPOPULATION Summary of Threat The human population has approximately tripled in the last 50 years. If the number continues to increase, it must eventually reach the point where the Earth can no longer produce enough food and other resources for everyone, and mass starvation or other so-called corrections will result. No one knows exactly when that day will arrive, how many people the Earth can support, or what quality of life the majority will accept.

So What? After the invention of agriculture made it possible for large numbers of people to live near one another, the exchange of ideas favored proliferation of the arts and sciences. Unfortunately, not only ideas were exchanged; crowding also increases the opportunity for infectious disease transmission. Modern sanitation and public health policies have reduced the risk, but it remains one of the trade-offs of civilization. Many airborne diseases, such as tuberculosis, influenza, and measles, spread rapidly under conditions of crowding and poverty (Figure 6.1). Aging or nonexistent sewage systems in densely



Figure 6.1 A public health worker visits a slum in northern India. Overcrowding, poverty, and famine promote the spread of many diseases. As the human population grows larger, these conditions are expected to increase. Source: U.S. Centers for Disease Control and Prevention, Public Health Image Library.

populated urban slums and box cities promote outbreaks of waterborne disease. Population growth also has indirect effects; the already-faltering healthcare system in many countries will eventually be strained past the breaking point. History shows that deadly childhood diseases such as diphtheria tend to re-emerge when governments are unable to provide vaccination and other health services. On Earth Day 2009, somebody finally said it (again). Dr. Charles A. Hall, a systems ecologist at the State University of New York, reportedly told the media that “Overpopulation is the only problem.” Population pressure also increases the likelihood of violence—possibly including biological warfare and bioterrorism, although we can’t be certain, because there is no large-scale precedent for either. People under stress often increase their disease risk by turning to unsafe behaviors such as substance abuse, overeating, and indiscriminate sex. Finally, population growth is likely to exacerbate global warming, environmental pollution, and famine, all of which contribute to disease risk and a general reduction in quality of life.

Can’t Scientists Do Something about It? Reducing the population means lowering the birth rate or raising the death rate, and the latter is not an option. We can invent better birth control methods, but people must decide whether to use them. Another approach is to invent technologies that make limited resources go further. Farmers are learning to grow more food on less land, but efficiency has an upper limit. Engineers



can build smaller and smaller cars, powered by solar cells or windup keys. Architects can design tiny cubicle apartments, stacked hundreds of stories high, in which humans can work online or raise their families or sit around. Generations accustomed to this type of life might find it satisfactory for a while, but its very complexity invites disaster. At some point, a key resource would fail. Ultimately, if population growth continues, all must fail. Scientists are often better at describing problems than fixing them. For example, biologists recognize two reproductive strategies called r and K selection. The r stands for the rate of population growth, and K is carrying capacity—the density (a measure of crowding) at which population growth stops. When the density is low, and environmental conditions are unstable, an animal might have numerous babies and dump them into the world as quickly as possible. Most will die—often from random events such as weather—but in a good year they might get lucky. That is r selection. But when the density is high, and conditions are stable, it’s more efficient to have fewer offspring and invest more energy in each one, to enable them to compete effectively for scarce resources. That’s K selection. Strictly speaking, these terms do not apply to human societies, but the comparison seems irresistible. Having fifteen children and sending them out to beg on the street sounds like r selection, whereas having one child and sending her to Harvard sounds like K selection. But humans are not mice, and such behavior is not hardwired. Studies have shown, for example, that educating girls can reduce the birthrate (Chapter 7).

The Numbers Some authorities believe that the human population will stabilize at somewhere between 8 and 10 billion people (Case Study 6-1). Others predict that it will crash before reaching that level, perhaps restabilizing at about 1 billion. Others claim that continued population growth will alternate with smaller corrections. (A crash or Case Study 6-1: The World of 2050 correction means a large number of human In 2050, the global population will probadeaths, usually resulting from density-dependent bly exceed 9 billion—assuming that an factors such as famine, disease, or interpersonal asteroid or other cosmic “correction” violence.) doesn’t hit us first—and most people in According to a 2008 study, the declining poorer countries will live in urban slums. birthrate in the European Union will result in This pattern could make the conquest of zero population growth by 2015. But immigratuberculosis harder than ever, unless an effective vaccine is widely available by tion will continue, so the EU population is 2050. Water pollution and associated disexpected to increase from the present 495 million eases may also increase. If present trends to a maximum of 521 million in 2035 and then continue, about one-sixth of all humans decline to about 506 million in 2060. Meanwill live in India, with nearly as many in while, the birthrate in the United States is China, and the United States coming in higher than it has been in more than 40 years, third with nearly 400 million people. About with 4,265,555 births in 2006 and no upper half of the Amazon rain forest will be gone, limit in sight. together with the Alpine glaciers and most A total fertility rate (TFR) of 2.0 children of the world’s ocean fisheries and coral per woman is the replacement rate necessary to reefs. Many vehicles may still run on fossil maintain a population at the same level. In 1970, fuels, but not for long. The average global temperature will probably be about 7ºF the TFR in China was about 5.8 children per (4ºC) warmer than in 2008, and some woman, and the population was 820 million. By coastal areas will be under water. 1999, the population had risen to 1.3 billion, but the TFR had declined to 1.8 children per woman,



thanks to China’s controversial family planning policy. The Chinese government estimated that the first 30 years of this policy prevented 350 million to 400 million births that would otherwise have occurred. During the same time period, India also made some headway in slowing population growth. Between the mid-1960s and 1997, India’s TFR declined from 5.7 to 3.3 children per woman. But in 2008 the rate stood at about three children per woman. Infant mortality has also declined, and as a result, India’s population continues to grow. In nearby Bangladesh, one of the world’s poorest countries, TFR was 6.4 in 1970 and 3.6 in 2003, with further decline anticipated. Rates of birth and death vary from one part of Africa to another. Tunisia has had remarkable success, reducing fertility from 7 children per woman in 1950 to 2 in 2006. Southern Africa, like India, reduced its TFR from about 5.7 children per woman in 1960 to 3.3 in 2000. Some Middle Eastern countries have also joined in the global effort to slow the rate of population growth. Iran, for example, reduced its TFR from 6.5 children per woman in 1980 to 2.5 in 2002. Several others, including Yemen, Iraq, and the Palestinian territories, have seen little change in fertility, with an average of 5.5 children per woman in 2002.

Discussion Human population control is a touchy subject. Some readers interpret the phrase as a call for abortion, euthanasia, or genocide. But population control really means any action (or inaction) that influences the rate of population increase. The word “control” implies that somebody is in charge, but in most cases the process is more like an old-fashioned Ouija board. Nobody consciously pushes the planchette in one direction or another, but the net efforts of the participants determine the outcome. In everyday life, euphemisms tend to replace harsher terms for events that people in the midst of the action cannot ignore: the soldier’s “collateral damage,” the firefighter’s “full involvement,” the politician’s “ethnic cleansing,” the animal researcher’s “humane endpoint,” the demographer’s “Malthusian adjustment,” and the ecologist’s “population correction.” The latter term usually refers to something like mice or deer, not people. A population builds up to a high level, and then disease and famine take over. Most of the mice (or whatever) die, and everything is back to normal again. So when a respected ecologist in 2006 told an audience that the world would be better off with 10 percent of the present population, it should have been obvious that he was not advocating mass murder. He assumed that the audience knew what he meant—that the human population has grown beyond a sustainable level, and the world would be a more comfortable place for everyone if there were fewer of us. But the wire services jumped on the speech, and columnists around the world redefined the ecoterrorist movement to include academic scientists and advocates of zero population growth. Some commentators have even claimed that the ultimate goal of the environmental movement is to annihilate the human race. (Note how easy it would be to quote the last part of that sentence out of context.) At the other extreme, the media sometimes ignore outrageous statements about population control. In 1971, the Texas House of Representatives unanimously passed a resolution honoring Albert deSalvo (the Boston Strangler) for his unselfish service to mankind and the “unconventional” way he dealt with overpopulation. Rep. Tom Moore allegedly sponsored this resolution in order to prove that the legislators did not read carefully, and it would appear that he succeeded. It’s unlikely that any scientist, or anyone else, really wants to see billions of people die from famine and disease. On the contrary, most of us wish people would plan ahead and avoid that fate, but in some countries—including the United States—this just isn’t happening. Any discussion of



infectious disease comes back to population growth sooner or later, because a hungry, crowded world can expect frequent disease outbreaks.

Popular Culture In the 1973 movie Soylent Green, an overcrowded future world resorts to a particularly creepy form of cannibalism. Logan’s Run (1976) portrays a future with an easier solution: kill everyone over 30. In Red Planet (2000), humans deal with overpopulation by trying to establish a colony on Mars. But in 2006, the real fear finally surfaced in Children of Men, which depicts a future in which humans lose the ability to have children. It is probably a safe bet that most people find this outcome scarier than overcrowding. In Alexei Panshin’s 1968 novel Rite of Passage, “free birth” is among the most shocking of all socially irresponsible acts, and every child learns that war is a consequence of population pressure. Many science-fiction classics feature a depopulated Earth after a nuclear or biological holocaust. A more fanciful solution to crowding appears in Clifford Simak’s 1952 novel Ring Around the Sun: human mutants arise who have the ability to step through dimensional barriers and enter an infinite number of worlds with fertile soil, clean air, and no people. If only the real problem were that easy to solve. Other science-fiction treatments of overpopulation include Robert Silverberg’s 1970 short story A Happy Day in 2381 and his 1971 novel The World Inside; Ursula K. LeGuin’s 1985 utopian novel Always Coming Home; John Brunner’s classic 1968 Stand on Zanzibar; and James Blish’s 1967 A Torrent of Faces. Jonathan Swift probably started the ball rolling in 1729 with his satirical essay A Modest Proposal, which proposed that the Irish poor should eat their children. (The Irish potato crop had recently failed for the first time, but not the last.) The Old Testament (Judges 6:4–6) tells us how the Midianites multiplied in such numbers that they left no food or land for the Israelites. By the standards of the day, the solution was obvious: kill them! Gideon was a humble man who led a small but deceptively loud Israelite army to victory over a larger, less organized force that panicked and surrendered. The name Gideon originally meant “Destroyer,” but it has acquired other connotations. In a 1969 Star Trek episode, for example, Gideon is an overpopulated alien world where birth control is forbidden. Recognizing that crowding is making life intolerable, the leaders introduce a deadly disease to kill many of their people. Thus, in both stories, one influential group imposes a violent solution on all.

Point/Counterpoint P: Governments can’t control population growth. Only free people can do that. Having children is a fundamental human right, and no government that claims otherwise will last long. In a freemarket economy, population growth is self-correcting. Besides, the world isn’t full yet. Huge areas are not being used for anything. Once the polar ice melts, we will have even more arable land. We can bring water to the deserts and farm the oceans, and there will be plenty of food for everyone. CP: Yes, there was a nice “correction” in Ireland in 1847. The abundance of food enabled the population to grow rapidly for a few generations, and then a million people died horribly when one crop failed. Some parts of Africa are undergoing similar “corrections” today. Mass starvation and disease are fine ways to limit population growth if you are a rodent, but aren’t humans ethically bound to do better? And for the sake of future generations, please don’t wreck the deserts and oceans, too. P: It always comes back to Ireland, doesn’t it?



The Future Human population growth cannot continue indefinitely, but recent numbers suggest that the global population might stabilize before the quality of life becomes unbearable. Meanwhile, the forces of r selection appear to be maintaining their lead while family planning advocates struggle to keep up. According to a 2009 report, several countries (including China and the UK) use computer games to teach people about contraception. But just explaining the mechanical details of birth control may not be enough. Students also need to understand the long-term consequences of personal choice. Perhaps high school science teachers could make more effective use of computer games, such as Sim City, to dramatize the effects of overcrowding and resource depletion.

References and Recommended Reading Aitken, R. J., et al. “As the World Grows: Contraception in the 21st Century.” Journal of Clinical Investigation, Vol. 118, 2008, pp. 1330–1343. Austin, L. “Prof. Criticized for Overpopulation View.” Associated Press, 4 April 2006. Bennett, J. “Overpopulation Is the Problem.” BioScience, 1 February 2007. “Combat Climate Change with Fewer Babies—OPT Report.” News Release, Optimum Population Trust, 7 May 2007. Dahl, R. “Population Equation: Balancing What We Have with What We Need.” Environmental Health Perspectives, Vol. 113, 2005, pp. A599–A605. Francis, D. R. “‘Birth Dearth’ Worries Pale in Comparison to Overpopulation.” Christian Science Monitor, 14 July 2008. Gillespie, D., et al. “Unwanted Fertility among the Poor: An Inequity?” Bulletin of the World Health Organization, Vol. 85, 2007, pp. 100–107. “Highest U.S. Birth Rate in Four Decades.” United Press International, 9 January 2009. Hoffman, M. C. “Philippines in Struggle against Abortionist Population Control Initiative.” LifeSiteNews.com, 22 July 2008. Howard, G. “China’s Population Control a Sensible Measure.” Pitt News, 20 March 2008. “Low-Cost Female Condom Popular in Britain.” United Press International, 22 December 2008. Morrison, P. “Who Will Heed the Warnings on the Population Bomb?” Los Angeles Times, 5 September 1999. Mudie, L., et al. “Abuses under Population Policies.” Radio Free Asia, 12 July 2008. Murdock, D. “Extremists Want Better Living through Mass Death.” The Telegraph, 17 June 2006. Page, S. T., et al. “Advances in Male Contraception.” Endocrine Review, Vol. 29, 2008, pp. 465–493. “Population: End to Natural Demographic Growth in 2015.” European Social Policy, 9 September 2008. Prugh, T. “Women: Population’s Once and Future Key.” World Watch, 1 September 2008. Richey, W. “Supreme Court Declines to Hear Asylum Case Involving Forced Abortion.” Christian Science Monitor, 13 May 2008. “Scientists Work on Garbage for Gas.” United Press International, 24 July 2008. Shah, I. H., and V. Chandra-Mouli. “Inequity and Unwanted Fertility in Developing Countries.” Bulletin of the World Health Organization, Vol. 85, 2007, p. 86. Sinding, S. W. “The Great Population Debates: How Relevant Are They for the 21st Century?” American Journal of Public Health, Vol. 90, 2000, pp. 1841–1845. State University of New York. “Worst Environmental Problem? Overpopulation, ESF Faculty Says.” Press Release, 21 April 2009. “U.N. Adopts Plan to Slow Population.” Los Angeles Times, 3 July 1999. Wallace, B. “Debate Grows with Population.” Los Angeles Times, 7 May 2008.



TOO MUCH CARBON: GLOBAL CLIMATE CHANGE Summary of Threat Nearly everyone has heard that the world is becoming warmer and that carbon emissions from human industries may be largely responsible. Higher temperatures, rising sea levels, and changes in the distribution of rainfall may transform the world we take for granted. Not everyone believes that this is happening; a decade ago, the author was not entirely convinced. But as of 2009, the evidence is overwhelming. So What? One effect of global warming, probably not the worst, will be a change in the distribution of certain infectious diseases. As the Earth grows warmer, malaria may disappear from some regions while expanding its range in others. If people in the newly affected areas lack immunity, the health impact could be significant. The forecast is clearer for some other pathogens and parasites, such as dengue fever, which has already spread into previously dengue-free areas at higher elevations than in the past (Chapter 3), and at least one plant fungus, phoma stem canker of canola (Chapter 5). Other diseases that may become more prevalent in Europe or North America include chikungunya fever (Case Study 6-2), tickborne encephalitis, yellow fever, Chagas disease, hantavirus infections, and salmonellosis. Even the incidence of rabies may increase, as New World vampire bats move northward. Sadly, the lungworm parasite that infests the lungs of sheep has already expanded its range in Scotland, endangering the production of Case Study 6-2: Chikungunya in Italy haggis. Another minor but scary player is the famous brain-eating amoeba (Naegleria fowleri), In December 2007, the wire services which lives in warm lakes. picked up an unusual story. An outbreak of Can’t Scientists Do Something about It? As of 2009, most nations have signed the 1998 Kyoto Protocol (a treaty to limit greenhouse gas emissions), but the cost of implementation is an issue, and the United States has not yet ratified it. Meanwhile, a 2009 study by the U.S. National Oceanic and Atmospheric Administration (NOAA) concluded that reversing climate change will take over 1,000 years even if we can stop releasing greenhouse gases into the atmosphere. Measures to reduce emissions can slow the warming process and improve air quality, but the catch phrase “Stop global warming” is no longer an option if the NOAA model is correct. We may have waited too long, but that is no excuse for giving up. Perhaps the new mantra should be “Slow global warming.”

a dengue-like tropical disease called chikungunya—known as “chik” in countries where it is endemic—had occurred in the small Italian village of Castiglione di Cervia. More than 100 people became severely ill, with high fever, joint pain, and exhaustion. Chik, like dengue, has a low death rate; in 2005, a major chik epidemic infected 266,000 people on the island of Réunion, and about 200 died. But the 2007 Italian outbreak was the first known example in which a temperate region experienced a tropical disease outbreak as a clear result of global climate change. The tropical tiger mosquito, a chik vector, had colonized Italy about 10 years earlier, thanks to warmer winters. Then an Italian man visited India in 2007 and brought back chik, and the mosquitoes were waiting, along with the press of the world.



The Numbers A 2007 study in England showed that each child who is born represents a lifetime “social cost” of about £30,000 ($43,000 U.S.) in carbon emissions alone. By 2074, the UK population will increase by about 10 million, for a total social cost of over £300 billion ($430 billion U.S.). For other relevant numbers, we refer the reader to Al Gore’s 2006 documentary An Inconvenient Truth. No film or book can be 100 percent accurate, but his presentation is fair, and it gets the message across. See also Figure 6.2.

Discussion In Pygmalion (1913), George Bernard Shaw observed that the safest conversational topics were the weather and everybody’s health. It would appear that societal norms have changed, for these two topics now form the basis of a bitter debate about global climate change, in which each side claims that the other is ignoring scientific facts in favor of irrational fears. Suffice it to say that everyone’s worldview combines elements of both fact and belief; that the best available data appear to prove beyond any reasonable doubt that the Earth is in a warming trend; that said warming is partly the result of the greenhouse effect, in which carbon

Figure 6.2 Monthly mean atmospheric carbon dioxide at Mauna Loa Observatory, Hawaii. These data, measured as the mole fraction in dry air, constitute the longest record of direct measurements of CO2 in the atmosphere. Source: U.S. National Oceanic and Atmospheric Administration.



emissions from human activities trap heat near the surface; and that the resulting long-term global climate change is likely to affect human societies in a number of ways, not all of them known or knowable. In a previous book published in 2000, this author presented both sides of the global warming argument—at the publisher’s request, in the interest of balance. But a decade later, little doubt remains. The world’s climate is changing, and humans are at least partly responsible. Even if you live in a solar-powered cabin in the woods and drink from a lake, everything from the solar panels on the roof to the Sierra cup in your hand implies the existence of energy-guzzling technologies. Most of that energy comes from fossil fuel combustion, which creates greenhouse gases. In 2008, the University of Illinois conducted a poll of 3,146 qualified earth scientists and found that 90 percent agreed that average global temperatures have risen in the last 200 years. Moreover, 82 percent agreed that human activity has been a significant factor in global warming. Given the respondent population, this is an overwhelming consensus. It would be hard to find any issue on which 100 percent of scientists agree, because science is not religion, and certainty is a big word.

Popular Culture In a 1936 interview, the American climatologist Charles D. Reed (1875–1945) made the interesting observation that people in every era believe that the world is growing warmer.1 He attributed this tendency to the fact that snow seems deeper to a child than to an adult. Yet Reed also acknowledged a measurable warming trend. The issue had already been controversial for at least 40 years, since 1896, when Swedish physicist Svante Arrhenius (1859–1927) showed that the accumulation of CO2 in the atmosphere would trap heat near the Earth. Scientists began to take global warming seriously in the 1950s, and comic books kept pace. Strange Adventures (DC Comics) ran stories on global warming in April 1955 (“The Day the Sun Exploded”), January 1956 (“The Earth-Drowners”), and September 1958 (“The Menace of Saturn’s Rings”). Several motion pictures have explored global warming, including the 1995 quasi-blockbuster Waterworld. Critics complained that there is not enough water on Earth to submerge all the continents, but the message was clear enough: in a warmer world, ice will melt and sea levels will rise. In The Arrival (1996), an astronomer discovers that alien invaders who hate cold weather are responsible for global warming. Science fiction often employs artistic license to make a point; the 2004 movie Day After Tomorrow focuses on a real process rather than the aftermath, so it must compress the time frame of global climate change into a few days. It would be hard to get audiences to sit through a film in which a column of mercury rises slowly over a period of years or centuries. In Michael Crichton’s 2004 novel State of Fear, a scientist discovers that global warming is a hoax. As always, Crichton knew what the public wants to read about: evil doctors, dumb scientists, corrupt politicians, global conspiracies, and brave loners who know the truth. But the message is useful, because climatologists (like everyone else) may overstate their position on occasion.

The Future This book can add little to the voluminous literature on global warming and the future of the Earth. The climate will grow warmer, on average, and possibly less predictable, and people will suffer and adapt as they have always done. 1. “Records Reveal Iowa Gradually Getting Warmer” (Iowa Daily Press Bureau, 6 January 1936).



It is not clear if malaria will become a worldwide problem, because vector control and window screens have eliminated malaria from many regions that are already warm enough to sustain it. At the right stage of its life cycle, the malaria parasite can even be killed by heat. Thus, its future distribution may depend not only on continued public health effort—a separate problem— but also on daily temperature fluctuations that are harder to predict than simple averages. We will live in interesting times. Point/Counterpoint P: Climate change is natural, whether humans cause it or not. Species will go extinct and resources will be depleted, but other species and resources will replace them. Without such changes, the great extinctions and biodiversity explosions of the past would never have happened. When our coastal cities are submerged, scuba divers will have fun exploring them. Building sea walls and new cities will create jobs and eliminate slums. Man adapts. CP: Yes, change is natural and inevitable, and one day something else will dig up our fossils and try to figure out where the brain was located. This is all very interesting to think about. But disease and death are natural changes too, and yet we try to protect our children from needless suffering and give them the best world we can. Why have children, if we don’t care what happens to future generations?

References and Recommended Reading Bandyopadhyay, R., and P. A. Frederiksen. “Contemporary Global Movement of Emerging Plant Diseases.” Annals of the New York Academy of Sciences, Vol. 894, 1999, pp. 28–36. Bloom, J. “Is the World Ending, or What?” United Press International, 25 April 2002. Borenstein, S. “Two Greenhouse Gases on the Rise Worry Scientists.” Associated Press, 24 October 2008. Brown, H. “Reducing the Impact of Climate Change.” Bulletin of the World Health Organization, Vol. 85, 2007, pp. 824–825. Campbell-Lendrum, D., et al. “Global Climate Change: Implications for International Public Health Policy.” Bulletin of the World Health Organization, Vol. 85, 2007, pp. 235–237. Carcavallo, R. U. “Climatic Factors Related to Chagas Disease Transmission.” Memórias do Instituto Oswaldo Cruz, Rio de Janeiro, Vol. 94 (Suppl. 1), 1999, pp. 367–369. Chung, J. “A Tropical Virus Moves North.” Los Angeles Times, 29 December 2007. “Climate Change May Alter Malaria Patterns.” United Press International, 16 February 2009. Connor, S. “The Methane Time Bomb.” The Independent, 23 September 2008. “Disease Outbreaks Blamed on Climate Change.” Reuters, 12 June 2008. Evans, N., et al. “Range and Severity of a Plant Disease Increased by Global Warming.” Journal of the Royal Society Interface, Vol. 5, 2008, pp. 525–531. Gilbert, M., “Climate Change and Avian Influenza.” Revue Scientifique et Technique, Vol. 27, 2008, pp. 459–466. “Global Warming: Return of Vampire Bats?” Washington Post, 6 November 1989. “Global Warming Skeptics Target Students.” United Press International, 5 May 2008. Gore, Al. “An Inconvenient Truth: A Global Warning.” Hollywood, CA: Paramount Pictures, 2006, 96 min. (DVD). Gray, L. “Haggis at Risk from Global Warming.” The Telegraph, 10 August 2008. Gubler, D. J., et al. “Climate Variability and Change in the United States: Potential Impacts on Vector- and Rodent-borne Diseases.” Environmental Health Perspectives, Vol. 109 (Suppl. 2), 2001, pp. 223–233. Haines, A., et al. “Climate Change and Human Health: Impacts, Vulnerability, and Mitigation.” Lancet, Vol. 367, 2006, pp. 2101–2109. Harvell, C. D., et al. “Climate Warming and Disease Risks for Terrestrial and Marine Biota.” Science, Vol. 296, 2002, pp. 2158–2162.



Hebert, H. J. “Heavy Editing Is Alleged in Climate Testimony.” Associated Press, 24 October 2007. IGAD Climate Prediction and Applications Centre. “Climate Change and Human Development in Africa: Assessing the Risks and Vulnerability of Climate Change in Kenya, Malawi and Ethiopia.” Draft Report, United Nations Development Programme, 2007. “Italian Village Hosts Tropical Disease.” United Press International, 22 December 2007. Khasnis, A. A., and M. D. Nettleman. “Global Warming and Infectious Disease.” Archives of Medical Research, Vol. 36, 2005, pp. 689–696. Lehman, J. A., et al. “Effect of Hurricane Katrina on Arboviral Disease Transmission.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1273–1275. Martin, V., et al. “The Impact of Climate Change on the Epidemiology and Control of Rift Valley Fever.” Revue Scientifique et Technique, Vol. 27, 2008, pp. 413–426. Michel, R., et al. “Risk for Epidemics after Natural Disasters.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 785–786. Parry, M., et al. “Climate Change, Global Food Supply and Risk of Hunger.” Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, Vol. 360, 2005, pp. 2125–2138. Patz, J. A., et al. “The Effects of Changing Weather on Public Health.” Annual Review of Public Health, Vol. 21, 2000, pp. 271–307. Patz, J. A., and S. H. Olson. “Climate Change and Health: Global to Local Influences on Disease Risk.” Annals of Tropical Medicine and Parasitology, Vol. 100, 2006, pp. 535–549. Pinzon, J. E., et al. “Trigger Events: Enviroclimatic Coupling of Ebola Hemorrhagic Fever Outbreaks.” American Journal of Tropical Medicine and Hygiene, Vol. 71, 2004, pp. 664–674. Pogatchnik, S. “Belfast Environment Chief Bans Climate Change Ads.” Associated Press, 9 February 2009. “Poll: U.S. Not Panicked by Global Warming.” United Press International, 21 April 2008. Quarles, W. “Global Warming Means More Pests.” IPM Practitioner, Vol. 29, 2007, pp. 1–8. Reiter, P., et al. “Texas Lifestyle Limits Transmission of Dengue Virus.” Emerging Infectious Diseases, Vol. 9, 2003, pp. 86–89. Rose, J. B., et al. “Climate Variability and Change in the United States: Potential Impacts on Water- and Foodborne Diseases Caused by Microbiologic Agents.” Environmental Health Perspectives, Vol. 109 (Suppl. 2), 2001, pp. 211–221. Rosenthal, E. “As Earth Warms Up, Tropical Virus Moves to Italy.” New York Times, 23 December 2007. Rosenzweig, C., et al. “Attributing Physical and Biological Impacts to Anthropogenic Climate Change.” Nature, Vol. 453, 2008, pp. 353–358. “Salmon Disease Blamed on Warmer Climate.” United Press International, 14 June 2008. “Scientists Agree Human-Induced Global Warming Is Real, Survey Says.” ScienceDaily, 21 January 2009. Shulman, S., et al. “Smoke, Mirrors, and Hot Air: How ExxonMobil uses Big Tobacco’s Tactics to Manufacture Uncertainty on Climate Science.” Cambridge, MA: Union of Concerned Scientists, 2007, 68 pp. “Six Die from Brain-Eating Amoeba.” Associated Press, 28 September 2007. Smith, E. “Despite Awareness of Global Warming, Americans Concerned More About Local Environment.” News Release, University of Missouri, 26 March 2008. Sokolov, A., et al. “Probabilistic Forecast for 21st Century Climate Based on Uncertainties in Emissions (without Policy) and Climate Parameters.” Journal of Climate, 2009. Solomon, S., et al. “Irreversible Climate Change due to Carbon Dioxide Emissions.” Proceedings of the National Academy of Sciences, Vol. 106, 2009, pp. 1704–1709. Sutherst, R. W. “Global Change and Human Vulnerability to Vector-borne Diseases.” Clinical Microbiology Reviews, Vol. 17, 2004, pp. 136–173. Traynor, K. “Warming Earth Could Face New Flu, Disease Threats.” American Journal of Health System Pharmacy, Vol. 65, 2008, pp. 1112–1114. U.S. Environmental Protection Agency. “Climate Change and Public Health.” EPA 236-F-97-005, Office of Policy, Planning and Evaluation, October 1997. “U.S. Power Plant Carbon Emissions Zoom in 2007.” ENS, 18 March 2008. Walsh, B. “Can Climate Change Make Us Sicker?” Time, 4 April 2008. Watkins, K., et al. “Fighting Climate Change: Human Solidarity in a Divided World.” New York: United Nations Development Programme, Human Development Report, 2007/2008.



Watson, J. T., et al. “Epidemics after Natural Disasters.” Emerging Infectious Diseases, Vol. 13, 2007, pp. 1–5. World Health Organization. “New Global Effort to Eliminate Chagas Disease: Partners Set Out Strategy Against the ‘Kissing Bug’ Disease.” News Release, 3 July 2007.

NOT ENOUGH FOOD: FAMINE, PESTILENCE, DESTRUCTION, AND DEATH Summary of Threat Despite the successful Green Revolution of the 1960s and 1970s and more recent advances in agricultural technology, world hunger remains a widespread problem. In 2008 alone, an estimated 20 million people died from the effects of famine. Trends discussed in the two previous sections, human population growth and global warming, can only exacerbate this problem.

So What? Aside from the cost in human suffering, hunger and malnutrition are underlying factors in many infectious disease epidemics, particularly in the tropics. An immune system weakened by an inadequate diet often falls prey to infections that would not threaten a healthy person. In a famine, some people starve to death, but many more die from disease and other indirect consequences of food shortage. Starving people may also resort to actions they would otherwise abhor, such as killing their neighbors and stealing their food, or blaming a specific ethnic group for the crisis. War, in turn, often promotes conditions (such as mass migrations and crop damage) that result in more famine and more disease.

Can’t Scientists Do Something about It? Scientists work constantly to detect plant and animal disease outbreaks, eliminate vectors, and develop resistant crops, but the task of fighting world hunger falls largely to economists and heads of state. At present, the world produces enough food for everyone, thanks in part to new crops and technologies developed during the Green Revolution. The problem is unequal distribution, and science can’t do much about that. Also, prices are subject to the laws of supply and demand, and if the price of a staple food rises to the point where most local people are unable to buy it, growers or governments may export it instead, thus making the problem worse. In the notso-distant future, when the global food supply actually falls short of demand, the role of science may eclipse these concerns.

The Numbers According to a frequently quoted statistic, Europe has had at least 400 major famines in recorded history. China has fared even worse, with 1,828 major famines between 108 B.C. and A.D. 1911. Table 6.1 lists examples. Several sources report that one child starves to death (or dies of causes related to malnutrition) every 5 or 6 seconds in the early twenty-first century. If true, that means about 6 million



Table 6.1 Some Major Famines in Human History Date


Estimated Deaths from Famine

1601–03 1630–31 1693–94 1695–97 1702–04 1738–56 1770 1783 1845–49 1866–68 1876–78 1876–79 1896–1902 1907 1921–22 1936 1941 1958–61 1984–85 1996–98 1998–2004

Russia India France Estonia India Timbuktu India Iceland Ireland Finland India Northern China India China Russia China China China Ethiopia North Korea Congo

2 million 2 million 2 million 20% of the population 2 million Half the population 15 million 20% of the population 1 million 15% of the population 5 million 13 million 19 million 24 million 5 million 5 million 3 million 20 million 1 million 1.2 million 3.8 million

children die from starvation every year. But estimates of the total number of people (adults and children) who starve every year range from 5 million to 20 million or more. Part of the uncertainty results from the problem of defining causes “related” to malnutrition. If a child dies of measles because she was half-starved, does she also die of starvation? Is a death from new variant famine (Chapter 2) a death from HIV, or from hunger? Whatever the real numbers, they are too high. Discussion Throughout most of human history, wild fish and game populations were available as a hedge against famine. Survivalists still think they can live off the land after the Apocalypse. The problem is that there are far too many of us. For example, in 2008, the deer population of the United States reached a record level of 30 million —higher even than when the first Europeans got off the boat. But there were also about 300 million people in the United States in 2008. We can quibble about other wild resources, rabbits and berries and bark, but it is safe to conclude that the hunter-gatherer lifestyle is no longer practicable on a large scale. Fish? According to a 2006 study by an international research team, most of the world’s marine seafood populations are already in trouble and will collapse by 2050 as a result of overfishing, pollution, biodiversity loss, and—yes—climate change. The United Nations Food and Agriculture Organization (FAO) has warned for years that about 70 percent of fish species are in danger of collapse. “Collapse” does not mean that most edible seafoods will actually vanish, just that their numbers will decline by at least 90 percent, so that commercial fishing will no longer be viable (see Case Study 6-3, page 206).



Case Study 6-3: Aquaculture In the 1950s, people wanted to farm the oceans as a solution to world hunger. By the 1980s, the focus had shifted to aquaculture, defined as the cultivation of aquatic organisms in tanks, ponds, or offshore enclosures. Aquaculture has great potential, but it also creates certain problems. For example, farm-raised fish need to eat something, and the most valuable species (such as salmon) are carnivores that normally eat other fish. So aquaculturists feed them—you guessed it—wild fish harvested from the oceans. By one estimate, every kilogram of farmed fish requires about 6 kilograms of wild fish. Aquaculture also generates large amounts of organic waste that often finds its way into the ocean or groundwater. In some parts of the world, particularly Southeast Asia, offshore aquaculture has destroyed mangrove forests. But there is no turning back. By 2004, aquaculture already contributed about one-third of total world fisheries production.

Large-scale famine seldom occurs in nations that are wealthy enough to buy pesticides, develop genetically modified disease-resistant crops, rent other people’s bees, stockpile food for future use, invent robotic pollinators, and import whatever resources are in short supply. But anyone who watches the news must be aware that less prosperous societies, particularly in Africa, continue to suffer plagues of near-Biblical proportions. Foreign aid, when it comes, may be hampered by inefficient distribution or political problems.

Popular Culture

Bhabani Bhattacharya’s 1947 novel So Many Hungers vividly depicts the Bengal Famine of 1943. Some movies and books about overpopulation (page 197) are also about hunger, since the two conditions often go together. For the literature of the Irish Famine, see Chapter 5. In a gentler era, comic book publishers did their part. The May 1946 Aquaman (Adventure Comics) featured a story about world hunger, entitled “Four Fish to Fetch.” The August 1958 issue of Strange Adventures (DC Comics) addressed the same theme in “The Boy Who Saved the Solar System.” A common folktale motif in many cultures is “The Magic Cauldron,” usually a container that is always magically filled with food. In a popular X-Files episode, a fifteenth-century French peasant girl wishes for the three things everyone wants: a stout-hearted mule (transportation), a magic sack that is always full of turnips (food), and long life (long life). Transportation and food always seem to come first, but without the magic cauldron or sack or wok, the two will always be in conflict. Do we feed the mule, or eat it? Do we buy gasoline, hay, or milk?

Point/Counterpoint P: The world actually has a surplus of food, but governments pay farmers not to grow crops. If they grow too much, the market prices fall. There is no food shortage, just problems with distribution. Humanitarian aid is self-defeating anyway—remember what happened in Somalia in 1993. But genetically modified crops and better farming methods will soon make these developing countries self-sustaining. CP: Good idea in principle, but GM seeds are not available to most Third World farmers. Many can’t afford them, and others don’t know which ones to buy. They lose their farming skills and end up in debt. And if we just stop the food shipments, hundreds of millions more people will die. Someday that might be necessary, but not yet. Aside from humanity, there’s expediency. If one government doesn’t feed them, another will.



The Future The widespread use of high-yield genetically modified (GM) crops and livestock appears to be inevitable. This approach has hit a few snags (Chapter 5), and a 2009 study concluded that genetic engineering has failed thus far to produce higher crop yields. Some GM organisms are disease-resistant, however, and wider use of this technology might at least reduce the need for pesticides and antibiotics. Climate change may help farmers in some parts of the world (such as Canada) by extending the growing season, while further reducing the food supply in the tropics. But if food prices continue to rise, the Third World food price riots of 2007–2008 may provide the clearest glimpse of the future. During that crisis, developed nations pledged some $18 billion in food aid to poorer countries, but Newsweek reported in 2009 that most of the promised aid never materialized.

References and Recommended Reading Avery, D. T. “Must We Suffer through Global Famine Again?” Feedstuffs, 19 May 2008. Borenstein, S. “Overlooked in the Global Food Crisis: A Problem with Dirt.” Associated Press, 8 May 2008. Brown, L. R. “Why Ethanol Production Will Drive World Food Prices Even Higher in 2008.” Earth Policy Institute, 24 January 2008. Buerkle, T. “40 Countries Face Food Shortages Worldwide.” News Release, United Nations Food and Agriculture Organization, 9 October 2006. Charles, D. “Will a Warmer World Have Enough Food?” NPR.org, 29 October 2007. Clover, C. 2004. The End of the Line. London: Ebury. Clover, C. “Food Shortages: How Will We Feed the World?” The Telegraph, 22 April 2008. Edwards, P., and I. Roberts. “Transport Policy Is Food Policy.” Lancet, Vol. 371, 2008, p. 1661. “Europe, Brazil Pledge Sustainable Biofuels Development.” Environment News Service, 5 July 2007. Foroohar, R. “Hungry Again.” Newsweek, 30 January 2009. “Global Food Shortage a ‘Dangerous Threat.’” Farmers Guardian, 23 April 2004. Gurian-Sherman, D. “Failure to Yield: Evaluating the Performance of Genetically Engineered Crops.” Union of Concerned Scientists, April 2009. Haile, M. “Weather Patterns, Food Security and Humanitarian Response in Sub-Saharan Africa.” Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, Vol. 360, 2005, pp. 2169–2182. Krisberg, K. “Global Food Shortages, Rising Prices Threaten Public Health: Advocates Call for Food Aid Restructuring.” The Nation’s Health, 1 June 2008. Krugman, P. “Grains Gone Wild.” New York Times, 7 April 2008. Lawn, J. E., et al. “Countdown to 2015: Will the Millennium Development Goal for Child Survival Be Met?” Archives of Disease in Childhood, Vol. 92, 2007, pp. 551–556. Menon, R. “Famine in Malawi: Causes and Consequences.” United Nations Development Programme Occasional Paper, Human Development Report Office, 2007, 14 pp. Monbiot, G. “Manufactured Famine.” The Guardian, 26 August 2008. Myers, R. A., and B. Worm. “Rapid Worldwide Depletion of Predatory Fish Communities.” Nature, Vol. 423, 2003, pp. 280–283. Perry, A. “Ethiopia: Pain Amid Plenty.” Time, 6 August 2008. Prentice, A. “Fires of Life: The Struggles of an Ancient Metabolism in a Modern World.” Nutrition Bulletin, Vol. 26, 2001, pp. 13–27. Prentice, A., et al. “Insights from the Developing World: Thrifty Genotypes and Thrifty Phenotypes.” Proceedings of the Nutrition Society, Vol. 64, 2005, pp. 153–161. Rukuni, M. “Africa: Addressing Growing Threats to Food Security.” Journal of Nutrition, Vol. 132, 2002, pp. 3443S–3448S. Sachs, J. “How to End the Global Food Shortage.” Time, 24 April 2008.



Sachs, J. “Are Malthus’s Predicted 1798 Food Shortages Coming True?” Scientific American, 25 August 2008. Subasinghe, R., and D. Bartley. “Ensuring the Sustainability of Aquatic Production.” Rome: Food and Agriculture Organization of the United Nations, FAO Aquaculture Newsletter No. 31, 2004. United Nations World Food Programme. 2007. World Hunger Series: Hunger and Health. Rome: Earthscan, 212 pp. Verdin, J., et al. “Climate Science and Famine Early Warning.” Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, Vol. 360, 2005, pp. 2155–2168. Vidal, J., and T. Radford. “One in Six Countries Facing Food Shortage.” The Guardian, 30 June 2005. von Braun, J. “The World Food Situation: New Driving Forces and Required Actions.” Washington, D.C.: International Food Policy Research Institute Food Policy Report, December 2007, 27 pp. Walt, V. “The World’s Growing Food-Price Crisis.” Time, 27 Feb 2008. Worm, B., et al. “Impacts of Biodiversity Loss on Ocean Ecosystem Services.” Science, Vol. 314, 2006, pp. 787–790.

TOO MUCH FOOD: METABOLIC SYNDROME AND TYPE 2 DIABETES Summary of Threat Obesity and its associated diseases are among the most urgent health problems facing developed nations today—an irony that is not lost on the Third World, which has the opposite problem. Doctors are not certain if the famous “metabolic syndrome” even exists, but its component conditions are all too real: obesity, glucose intolerance, high blood pressure, high LDL cholesterol, and hardening of the arteries.

So What? Obese people are more likely than others to develop type 2 (adult onset) diabetes, which in turn is a major risk factor for tuberculosis, melioidosis, and other infectious diseases. Obesity itself is a risk factor for influenza and certain bacterial infections, because it tends to suppress the immune system. (A recent study showed that overweight people are less likely than others to die of pneumonia, but only because they are more likely to die from noninfectious conditions such as heart disease.) Many overweight children become overweight, diabetic, chronically unhealthy adults. Yet studies show that parents often fail to realize that their children are fat. Many are in denial; in 2008, an obese woman made headlines by explaining that it was impossible for her to lose weight because fresh vegetables were too expensive. Besides compromising personal health, a mutually reinforcing culture of fatness imposes one more burden on the already overstrained healthcare system. According to a 2000 Surgeon General’s report, the direct and indirect cost of obesity was $117 billion each year for the U.S. alone. More recent estimates are even higher.

Can’t Scientists Do Something about It? Scientists can study genetic and cultural factors that contribute to obesity, and publish the results. We can try to scare people by telling them what food is doing to their arteries and livers and kidneys. We can browbeat fast-food restaurant chains into reducing the trans fat content of



their deep-fried glop, and we can advise school districts to serve salads. But individuals are ultimately responsible for their own food choices and exercise habits.

The Numbers Diabetes drug spending in the United States rose from $6.7 billion in 2001 to $12.5 billion in 2007. As of 2009, nearly 20 million Americans have type 2 diabetes. Denial may complicate the problem of obesity. In 2005–2006, the U.S. Centers for Disease Control and Prevention determined that 34 percent of American adults were obese when weighed, but only 26 percent admitted to being obese when interviewed by telephone.

Discussion Obesity is largely a matter of eating too much and exercising too little. All living things that are capable of liking anything seem to like food, and they tend to overeat when a surplus presents itself. Humans in developed nations have more than a surplus; we are constantly bombarded with images of food that is fatter, sweeter, more brightly colored, and more readily available than anything in nature—what ethologists call a supernormal stimulus. Our ancestor Homo erectus would have loved a deep-dish pizza, which even today conjures images of a predator tearing into the belly of a still-warm quarry whose organs and blood and stomach contents are spilling onto the veldt. But greed can’t be the whole story, because some people also seem to assimilate food more efficiently than others. Most people will never weigh 500 or 1,000 pounds, regardless of how much they eat. Obesity, particularly morbid obesity, is often associated with type 2 diabetes (Case Study 6-4). But does obesity predispose to diabetes, or is it the other way around? Or does a third factor cause both? According to one theory, “thrifty genes” that favor survival under famine conditions also promote obesity and diabetes. According to another theory, these two conditions, plus several others—high blood pressure, insulin resistance in the liver, high cholesterol, and hardening of the arteries—constitute something called “metabolic syndrome.” Some experts deny that there is any such thing; in 2005, the American Diabetes Association and the European Association for the Study of Diabetes issued a joint position Case Study 6-4: Gastric Banding statement to the effect that metabolic syndrome and Diabetes is nothing more than the sum of its parts. Even so, those parts are conditions best avoided. A 2008 study produced the latest in a mountain of reports that support the same concluA number of studies have implicated causal sion: Most (not all) cases of type 2 diabetes factors other than genetics or gluttony. Several appear to result from obesity, and losing viruses appear to trigger diabetes, including the weight is a good way to control diabetes and arenavirus that causes lymphocytic choriomeninreduce the need for medication. One group gitis (Chapter 3). One type of airborne adenovirus of obese patients with diabetes had gastric appears to make fat cells multiply. Arsenic, diet banding surgery while a second group had soda, fast food, tobacco, the absence of ulcerconventional diabetes therapy with emphacausing bacteria (Helicobacter pylori) in the sis on lifestyle change. At follow-up, 73 perstomach, the absence of intestinal parasites, and cent of the surgical-banding group achieved various pollutants of air, water, and soil have all remission of diabetes, as compared with 13 been proposed as explanations for obesity or diapercent of the conventional-therapy group. betes. But some 17 million American dogs are



obese, too, yet few of them live on diet soda and fast food or use tobacco, and none of them are genetically related to their owners. (About 1 dog in 300 develops diabetes, as does 1 cat in 400.) Popular Culture Some preachers have used HIV or syphilis to illustrate the wages of sin, yet they rarely dismiss diabetics or quadruple bypass patients with the same sniff. Lust, gluttony, and sloth are all among the seven deadly sins, the last time we checked; yet hardly anyone seems to blame people for illnesses that result from overeating or lack of exercise. Benjamin Franklin’s insightful conversation with his gouty big toe proves once again what a genius he was: FRANKLIN. Eh! Oh! Eh! What have I done to merit these cruel sufferings? GOUT. Many things; you have ate and drank too freely, and too much indulged those legs of yours in their indolence.2

Gout seems to be less common now than it was in Franklin’s day, or at least less highly publicized than diabetes, which afflicts a similar population—essentially, overweight people who are susceptible by heredity, and who eat too much and exercise too little. Diabetes has been a theme in at least 25 motion pictures, notably Steel Magnolias (1989), The Godfather III (1990), Chocolat (2000), and It Runs in the Family (2003). The 2004 movie Super Size Me is about fast food. The Nutty Professor (1996) and Norbit (2007) feature Eddie Murphy in a fat suit. Traditional folk remedies for diabetes in North America and northern Europe include powdered mice, chickweed and comfrey tea, wormwood, geranium root, dandelion, boiled nettles, horsetail, Spanish moss, bugle weed, yarrow, sumac, huckleberry root, sage, and mullein leaf tea. Nonplant remedies included sulfur and molasses, goat’s milk, buttermilk, honey, and vinegar. Extreme cures included drinking one’s own urine or being bitten by a venomous snake. In Irish folklore, walking on “hungry grass” was said to cause weakness and diabetes. Some sources identify it as creeping bentgrass (Agrostis stolonifera), which now grows on golf courses throughout the world without reported adverse health effects. Others claim that “hungry grass” referred to a patch of cursed grass near a body that was buried without benefit of clergy. Point/Counterpoint P: It’s normal for the most successful, desirable people to be well fed. Having plenty of food has always been a sign of high social status. Look at Polynesian cultures. Look at the Venus of Willendorf. Look at the voluptuous women in Rubens’ paintings. Western culture is hung up on a preadolescent ideal of beauty. CP: Agreed! But we are talking about health, not beauty. Most (not all) overweight people are risking their health and their children’s health. Do they really enjoy watching an obese mother and daughter on a television ad, discussing their favorite glucose meters or stomach-stapling procedures? The Future The medical and sociological issues related to obesity will not go away in the foreseeable future, but it is important to remember that overeating is not a problem for everyone. Many people 2. Benjamin Franklin, Dialog Between Franklin and the Gout (1780).



love food and accept being heavy as a normal part of life. One question that researchers need to answer is why many of these people develop diabetes and heart disease, while others stay healthy.

References and Recommended Reading Albright, A. “What is Public Health Practice Telling Us about Diabetes?” Journal of the American Dietetic Association, Vol. 108 (Suppl. 4), 2008, pp. S12–18. Altman, B., and A. Bernstein. 2008. Disability and Health in the United States, 2001–2005. Hyattsville, MD: National Center for Health Statistics, 89 pp. Amar, S., et al. “Diet-Induced Obesity in Mice Causes Changes in Immune Responses and Bone Loss Manifested by Bacterial Challenge.” Proceedings of the National Academy of Sciences (U.S.), 12 December 2008. Benjamin, S. E., et al. “Obesity Prevention in Child Care: A Review of U.S. State Regulations.” BMC Public Health, Vol. 8, 2008, p. 188. Biddinger, S. B., et al. “Hepatic Insulin Resistance Is Sufficient to Produce Dyslipidemia and Susceptibility to Atherosclerosis.” Cell Metabolism, Vol. 7, 2008, pp. 125–134. Brownell, K. D., and D. Yach. “Lessons from a Small Country about the Global Obesity Crisis.” Globalization and Health, Vol. 2, 2006, p. 11. Chang, P.-C., et al. “Association Between Television Viewing and the Risk of Metabolic Syndrome in a Community-based Population.” BMC Public Health, Vol. 8, 2008, p. 193. Chowdhury, P., et al. “Surveillance of Certain Health Behaviors among States and Selected Local Areas— United States, 2005.” MMWR Surveillance Summaries, Vol. 56, 2007, pp. 1–164. Coronado, G. D., et al. “Attitudes and Beliefs among Mexican Americans about Type 2 Diabetes.” Journal of Health Care for the Poor and Underserved, Vol. 15, 2004, pp. 576–588. DeNoon, D. J. “Fat Fear Survey: Most Would Trade Family, Health, Wealth to Avoid Obesity.” WebMD, 18 May 2006. “Diabetes May Increase Risk of Developing TB.” Reuters, 15 July 2008. “Diabetes Rate Doubles in U.S. in Last 10 Years.” Associated Press, 30 October 2008. Dixon, J. B., et al. “Adjustable Gastric Banding and Conventional Therapy for Type 2 Diabetes: A Randomized Controlled Trial.” JAMA, Vol. 299, 2008, pp. 316–323. Drescher, K. M., and S. M. Tracy. “The CVB and Etiology of Type 1 Diabetes.” Current Topics in Microbiology and Immunology, Vol. 323, 2008, pp. 259–274. “Expert: Obesity is Epidemic of Our Time.” United Press International, 13 November 2008. Fee, M. “Racializing Narratives: Obesity, Diabetes, and the ‘Aboriginal’ Thrifty Genotype.” Social Science and Medicine, Vol. 62, 2006, pp. 2988–2997. “Hypereating Drives Many to Consume When Not Hungry.” Associated Press, 21 April 2009. Jaeckel, E., et al. “Viruses and Diabetes.” Annals of the New York Academy of Sciences, Vol. 9, 2002, pp. 7–25. Kahn, R., et al. “The Metabolic Syndrome: Time for a Critical Reappraisal.” Diabetes Care, Vol. 28, 2005, pp. 2289–2304. Ko, G. T., and J. C. Chan. “Burden of Obesity—Lessons Learnt from Hong Kong Chinese.” Obesity Reviews, Vol. 9, Suppl. 1, 2008, pp. 35–40. Kolata, G. “Overweight People Found Less Likely to Die from Some Diseases.” New York Times, 7 November 2007. Krasnoff, J. B., et al. “Health-related Fitness and Physical Activity in Patients with Nonalcoholic Fatty Liver Disease.” Hepatology, Vol. 47, 2008, pp. 1158–1166. Levine, S., and R. Stein. “Childhood Obesity Threat to Future Health, Longevity.” Washington Post, 20 May 2008. Meetoo D., et al. “An Epidemiological Overview of Diabetes Across the World.” British Journal of Nursing, Vol. 16, 2007, pp. 1002–1007. “Obesity and Immunity Linked.” United Press International, 5 February 2008. O’Connell, J. “Even a Thin Person Can Get Diabetes.” MSNBC.com, 29 May 2008. “Over the Long Haul, Most Americans Will be Fat, Long-term Study Suggests.” Associated Press, 4 October 2005.



Park, A. “Study: Diabetes Linked to Cognitive Decline.” Time, 5 January 2009. Penn, L., et al. “Participants’ Perspective on Maintaining Behaviour Change: A Qualitative Study within the European Diabetes Prevention Study.” BMC Public Health, Vol. 8, 2008, p. 235. Santos, A. C., et al. “Gender, Socio-economic Status and Metabolic Syndrome in Middle-aged and Old Adults.” BMC Public Health, Vol. 8, 2008, p. 62. Schulte, P. A., et al. “A Framework for the Concurrent Consideration of Occupational Hazards and Obesity.” Annals of Occupational Hygiene, Vol. 52, 2008, pp. 555–566. Schwartz, M. B., et al. “The Influence of One’s Own Body Weight on Implicit and Explicit Anti-Fat Bias.” Obesity (Silver Spring), Vol. 14, 2006, pp. 440–447. Smith, A. G., et al. “Diet-Induced Obese Mice Have Increased Mortality and Altered Immune Responses When Infected with Influenza Virus.” Journal of Nutrition, Vol. 137, 2007, pp. 1236–1243. Speakman, J. R. “Thrifty Genes for Obesity and the Metabolic Syndrome—Time to Call Off the Search?” Diabetes and Vascular Disease Research, Vol. 3, 2006, pp. 7–11. Uauy, R., and E. Diaz. “Consequences of Food Energy Excess and Positive Energy Balance.” Public Health and Nutrition, Vol. 8, 2005, pp. 1077–1099. Vasan, R. S., et al. “Estimated Risks for Developing Obesity in the Framingham Heart Study.” Annals of Internal Medicine, Vol. 143, 2005, pp. 473–480. “Western Diet Boosts Global Heart Attack Risk 30%.” HealthDay News, 20 October 2008. Willey, J. “Obesity Bug You Can Catch.” Daily Express, 26 January 2009. Wu, M. S., et al. “A Case-Control Study of Association of Helicobacter pylori Infection with Morbid Obesity in Taiwan.” Archives of Internal Medicine, Vol. 165, 2005, pp. 1552–1555. Yach, D., et al. “Epidemiologic and Economic Consequences of the Global Epidemics of Obesity and Diabetes.” Nature Medicine, Vol. 12, 2006, pp. 62–66. Yang, Z., and A. G. Hall. “The Financial Burden of Overweight and Obesity among Elderly Americans: the Dynamics of Weight, Longevity, and Health Care Costs.” Health Services Research, Vol. 43, 2008, pp. 849–868.

TOO MANY SICK PEOPLE: THE HEALTHCARE CRISIS Summary of Threat Despite advances in medical science, the healthcare available on an everyday basis in the United States is often unaffordable (even with insurance), inaccessible, and substandard. Other countries have similar problems, but as of 2009, the United States claims the dubious honor of being the only developed nation that lacks some form of universal healthcare. The U.S. infant mortality rate is also among the highest in the developed world.

So What? If people with AIDS, tuberculosis, and other contagious diseases cannot afford their medication, all of society suffers. If vaccine shortages interfere with childhood immunization programs, or if families cannot afford to pay their doctors, or if they avoid their doctors because of perceived inadequate care, deadly childhood diseases may return. If physicians overprescribe antibiotics as a quick fix, the problem of drug-resistant bacteria will become worse. And if hospitals neglect sanitation, the death toll from hospital-acquired infections will continue to rise. Another aspect of the healthcare crisis is the allocation of research funding to popular programs (such as the war on bioterrorism) at the expense of real and present threats. In a 2007 Gallup poll to identify the most urgent U.S. health problems, the leading contenders were access and cost (Table 6.2).



Table 6.2 Most Urgent Health Problems, United States, 2007 Problem

Percentage of Respondents Saying This Was the Most Urgent

Access Cost Cancer Obesity AIDS Diabetes Heart disease Finding cures Flu Drug/alcohol abuse Smoking Bioterrorism Other No opinion

30 26 14 10 2 2 1 1 1 1